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1.
J Mater Chem B ; 2020 Feb 05.
Artigo em Inglês | MEDLINE | ID: mdl-32022083

RESUMO

Analysis of circulating tumor cells (CTCs) can provide significant clinical information for tumors, which has proven to be helpful for cancer diagnosis, prognosis monitoring, treatment efficacy, and personalized therapy. However, CTCs are an extremely rare cell population, which challenges the isolation of CTCs from patient blood. Over the last few decades, many strategies for CTC detection have been developed based on the physical and biological properties of CTCs. Among them, nanostructured interfaces have been widely applied as CTC detection platforms to overcome the current limitations associated with CTC capture. Furthermore, aptamers have attracted significant attention in the detection of CTCs due to their advantages, including good affinity, low cost, easy modification, excellent stability, and low immunogenicity. In addition, effective and nondestructive release of CTCs can be achieved by aptamer-mediated methods that are used under mild conditions. Herein, we review some progress in the detection and release of CTCs through aptamer-functionalized nanostructured interfaces.

2.
J Obstet Gynaecol Res ; 46(3): 451-458, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32003122

RESUMO

AIM: To explore the clinical effect of endometrial injury (EI) on the third day of the menstrual cycle before frozen-thawed embryo transfer (frozen-thawed ET) on patients experienced two or more implantation failures. METHODS: A total of 200 patients who suffered at least two failed hormone-replacement therapies and frozen-thawed ET were randomly divided into two groups: EI group and control group (n = 100 in each group). Patients in the EI group received local EI with a Pipelle catheter on the third day of the menstrual cycle before frozen-thawed ET. Primary outcomes were live birth, clinical pregnancy and implantation rates. Secondary outcomes were biochemical, multiple and ectopic pregnancy rates and abortion rates. RESULTS: The rate of live birth in EI group (51.00%) was significantly higher than that of control group (36.00%) (P = 0.032). Clinical pregnancy and implantation rates in EI group were significantly higher comparing to control group (64.00% vs 48.00%, P = 0.023 and 46.74% vs 30.11%, P = 0.001). The rate of multiple pregnancy in EI group (37.50%) was significantly higher than that of control group (18.75%) (P = 0.031). No significant difference in ectopic pregnancy rate and abortion rate was observed between EI group and control group. CONCLUSION: Applying EI to patients experienced two or more implantation failures on the third day of the menstrual cycle before frozen-thawed ET can improve clinical outcomes.

3.
Reprod Sci ; 2020 Jan 28.
Artigo em Inglês | MEDLINE | ID: mdl-31994002

RESUMO

lncRNA NR2F1-AS1 has been reported to be upregulated in hepatocellular carcinoma and plays oncogenic roles. Through the analysis of TCGA dataset, we observed the downregulation of NR2F1-AS1 in cervical squamous cell carcinoma (CSCC). This study was performed to analyze the functionality of NR2F1-AS1 in CSCC. It was observed that NR2F1-AS1 was significantly downregulated in tumor tissues than in paired non-tumor tissues in CSCC patients. Levels of NR2F1-AS1 decreased with increased in clinical stages. NR2F1-AS1 can directly interact with miR-17. Overexpression experiments showed that NR2F1-AS1 and miR-17 have no significant effects on the expression of each other. Interestingly, NR2F1-AS1 overexpression led to the upregulation of SIK1, a target of miR-17. Transwell assay analysis revealed decreased invasion and migration rates of CSCC cells after NR2F1-AS1 and SIK1 overexpression. miR-17 overexpression played an opposite role and reduced the effects of NR2F1-AS1 and SIK1 overexpression. Therefore, NR2F1-AS1 regulates miR-17/SIK1 axis to suppress the invasion and migration of CSCC cells.

4.
Kaohsiung J Med Sci ; 36(2): 114-121, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31688986

RESUMO

To screen the key circulating microRNAs (miRNAs) involved in missed abortion (MA) and explore their role in MA process. We examined the miRNA profile from the serum of three MA patients and three early pregnancy induced abortion patients (controls) by next-generation sequencing. We analyzed the target genes of the differentially expressed (DE) miRNAs to analyze the function and pathway enrichment using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes, respectively. We validated five candidate miRNAs by real time-qPCR. Integrated miRNA-mRNA-pathway network analysis was performed to show the interaction network of the candidate miRNAs and their target genes of interest with the involved pathways. It was observed that 227 miRNAs were differently expressed between the MA group and the early pregnancy control group, with 58 miRNAs downregulated and 169 miRNAs upregulated in the MA group. Real-time qPCR results revealed that expression of the five candidate miRNAs, namely hsa-miR-22-3p, hsa-miR-145-3p, hsa-miR-107, hsa-miR-361-3p, and hsa-miR-378c, was consistent with the miRNA data obtained by sequencing. Integrated miRNA-mRNA-pathway network analysis illustrated that target genes of the candidate miRNAs were mainly involved in the PI3K-Akt signaling pathway, HIF-1 signaling pathway, and VEGF signaling pathway, which would have potential significance in pregnancy and MA. We are the first to reveal the DE miRNAs involved in MA and illustrate their functional interaction network. These results might provide potential circulating biomarkers and new therapeutic targets for MA.

5.
Exp Ther Med ; 18(2): 1291-1298, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31363373

RESUMO

An accumulation of evidence has demonstrated that abnormal microRNA (miRNA or miR) expression is associated with different types of cancer, including endometrial cancer (EC). The dysregulation of miRNAs may serve important roles in the development and progression of EC by regulating multiple aggressive biological behaviors, including cell proliferation, apoptosis, metastasis and angiogenesis. An in-depth understanding of the miRNAs associated with EC initiation and progression may be crucial for identifying successful therapeutic techniques. miR-873 has been demonstrated to be dysregulated in different types of cancer. However, the expression status and regulatory roles of miR-873 are yet to be elucidated in EC. In the present study, reverse transcription-quantitative PCR was carried out to detect miR-873 expression in EC tissues and cell lines. Cell Counting Kit-8 and in vitro invasion assays were utilized to determine the influence of miR-873 on the proliferation and invasion of EC cells. miR-873 expression was revealed to be downregulated in EC tissues and cell lines. Decreased miR-873 expression was significantly associated with International Federation of Gynecology and Obstetrics stage and lymph node metastasis of patients with EC. Functional assays revealed that resumed miR-873 expression suppressed the proliferation and invasion of EC cells. Additionally, hepatoma-derived growth factor (HDGF) was indicated to be a direct target gene of miR-873 in EC cells. HDGF was highly expressed in EC tissues and inversely correlated with miR-873 expression. HDGF silencing also imitated the tumor-suppressor activity of miR-873 overexpression in EC cells. A series of rescue experiments identified that recovered HDGF expression hindered the anti-proliferative and anti-invasive roles of miR-873 upregulation in EC cells. In conclusion, the present study indicated that miR-873 serves an important role as a tumor suppressor in EC development by directly targeting HDGF. The results may provide a novel insight into clinical treatments, which can be used to prevent EC aggression.

6.
Oncol Lett ; 18(3): 2861-2868, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31452765

RESUMO

Ovarian malignancies are commonly diagnosed cancers of the female reproductive system. Recent studies have revealed that long non-coding RNAs (lncRNAs) can regulate a variety of oncological processes. In the present study, ovarian cancer expression datasets were searched in the GEO database using the GPL570 platform. Differential lncRNA expression between normal ovarian tissues and ovarian tumors were analyzed using the R package 'limma', and patient prognosis was accessed using the package 'survival'. Four databases, GSE14001, GSE18520, GSE38666 and GSE40595, were used for the analysis. A total of 64 lncRNAs were highly expressed and 4 were downregulated within these four databases. Prognostic analysis of the 68 lncRNAs in the four databases was performed, and revealed that the expression of long intergenic non-protein coding RNA 1627 (LINC01627) was negatively associated with patient prognosis in GSE19829 and GSE62193; there was no association between LINC01627 expression and patient's prognosis in GSE18520 or GSE63885. To investigate the proposed association between LINC01627 and patient prognosis, meta-analysis revealed that the total hazard ratio was 1.38 and the 95% confidence interval was between 1.04 and 1.83. Subgroup analysis revealed that LINC01627 may predict patient prognosis in high-grade, advanced and serous epithelial ovarian cancer, which was a risk factor for prognosis. Further assessment was performed in clinical samples and ovarian cancer cells, where the knockdown of LINC01627 inhibited the proliferative and migratory capacities of HO8910 and HEY cells. Collectively, the present results suggested that lncRNA LINC01627 may serve an oncogenic role in the development of epithelial ovarian tumors.

8.
Biol Res ; 52(1): 33, 2019 Jun 29.
Artigo em Inglês | MEDLINE | ID: mdl-31255182

RESUMO

BACKGROUND: Studies have shown that cancer susceptibility candidate 11 (CASC11), a newly discovered long non-coding RNA (lncRNA), was aberrantly overexpressed in hepatic carcinoma, gastric cancer and colorectal cancer. However, its effects on cervical cancer has been kept unknown up to now. The present study was aimed to investigate the relationship between lncRNA CASC11 and cervical cancer and further explore the mechanism of CASC11 effect on cervical cancer progression. MATERIALS: Quantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the expressions of CASC11 in cancerous and adjacent normal tissues of patients with cervical cancer as well as in cell lines. The proliferation, migration, invasion and apoptosis were assayed after transfecting the cell with si-CASC11 or pcDNA3.1-CASC11. TOP/FOP-Flash luciferase reporter assay and western blot were used to analysis the activation of Wnt/ß-catenin signaling pathway. Si-CASC11-transfected HeLa cells were subcutaneously inoculated into male athymic (nude) mice to investigate the effect of CASC11 on the tumor formation. RESULTS: We discovered that CASC11, the expression of which was positively associated with the tumor size and the FIGO staging and negatively related to the patients' survival rate, was up-regulated in the cervical cancer tissues and cell lines. Silencing CASC11 inhibited the proliferation, migration as well as invasion and promoted the cell apoptosis. Conversely, overexpression of CASC11 facilitated the cancer cell's proliferation, migration and invasion ability and suppressed the apoptosis. Further study showed that CASC11 promoted the migration and invasion of cervical cancer cells by activating Wnt/ß-catenin signaling pathway and silencing CASC11 inhibited the tumor growth in vivo. CONCLUSION: Our study demonstrated that CASC11 promoted the cervical cancer progression by activating Wnt/ß-catenin signaling pathway for the first time, which provides a new target or a potential diagnostic biomarker of the treatment for cervical cancer.


Assuntos
Predisposição Genética para Doença , MicroRNAs/genética , Neoplasias do Colo do Útero/genética , Neoplasias do Colo do Útero/patologia , Via de Sinalização Wnt/genética , beta Catenina/genética , Animais , Apoptose/genética , Proliferação de Células/genética , Progressão da Doença , Feminino , Citometria de Fluxo , Estudo de Associação Genômica Ampla , Humanos , Camundongos , Infecções por Papillomavirus/complicações , Neoplasias do Colo do Útero/virologia
9.
Biol. Res ; 52: 33, 2019. tab, graf
Artigo em Inglês | LILACS-Express | ID: biblio-1019498

RESUMO

Abstract Background: Studies have shown that cancer susceptibility candidate 11 (CASC11), a newly discovered long non-coding RNA (lncRNA), was aberrantly overexpressed in hepatic carcinoma, gastric cancer and colorectal cancer. However, its effects on cervical cancer has been kept unknown up to now. The present study was aimed to investigate the relationship between lncRNA CASC11 and cervical cancer and further explore the mechanism of CASC11 effect on cervical cancer progression. Materials: Quantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the expressions of CASC11 in cancerous and adjacent normal tissues of patients with cervical cancer as well as in cell lines. The proliferation, migration, invasion and apoptosis were assayed after transfecting the cell with si-CASC11 or pcDNA3.1-CASC11. TOP/FOP-Flash luciferase reporter assay and western blot were used to analysis the activation of Wnt/β-catenin signaling pathway. Si-CASC11-transfected HeLa cells were subcutaneously inoculated into male athymic (nude) mice to investigate the effect of CASC11 on the tumor formation. Results: We discovered that CASC11, the expression of which was positively associated with the tumor size and the FIGO staging and negatively related to the patients' survival rate, was up-regulated in the cervical cancer tissues and cell lines. Silencing CASC11 inhibited the proliferation, migration as well as invasion and promoted the cell apoptosis. Conversely, overexpression of CASC11 facilitated the cancer cell's proliferation, migration and invasion ability and suppressed the apoptosis. Further study showed that CASC11 promoted the migration and invasion of cervical cancer cells by activating Wnt/β-catenin signaling pathway and silencing CASC11 inhibited the tumor growth in vivo. Conclusion: Our study demonstrated that CASC11 promoted the cervical cancer progression by activating Wnt/β-catenin signaling pathway for the first time, which provides a new target or a potential diagnostic biomarker of the treatment for cervical cancer.

10.
Thromb Haemost ; 118(12): 2064-2073, 2018 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-30453347

RESUMO

Pre-eclampsia (PE) is a chronic inflammatory disease in pregnancy, which is associated with enhanced blood coagulation and high thrombotic risk. To date, the mechanisms underlying such an association are not fully understood. Previous studies reported high levels of plasma deoxyribonucleic acid (DNA) in PE women, but the cellular source of the circulation DNA remains unknown. In this study, we tested the hypothesis that activated neutrophils undergoing cell death, also called NETosis, may be responsible for the elevated plasma DNA levels in PE women. We analysed plasma samples from non-pregnant, normal pregnant and PE women and found high levels of double-stranded DNA, myeloperoxidase (an abundant neutrophil granular enzyme) and histones (the major nucleosome proteins) in PE-derived samples, indicating increased NETosis in the maternal circulation. The high plasma DNA levels positively correlated with enhanced blood coagulation in PE women. When isolated neutrophils from normal individuals were incubated with PE-derived plasma, an elevated NETosis-stimulating activity was detected. Further experiments showed that endothelial micro-particles, but not soluble proteins, in the plasma were primarily responsible for the NETosis-stimulating activity in PE women. These results indicate that circulating micro-particles from damaged maternal endothelium are a potent stimulator for neutrophil activation and NETosis in PE women. Given the pro-coagulant and pro-thrombotic nature of granular and nuclear contents from neutrophils, enhanced systemic NETosis may represent an important mechanism underlying the hyper-coagulability and increased thrombotic risk in PE.


Assuntos
Coagulação Sanguínea , DNA/sangue , Ativação de Neutrófilo , Neutrófilos/imunologia , Pré-Eclâmpsia/imunologia , Adulto , Idoso , Apoptose , Células Cultivadas , Armadilhas Extracelulares/metabolismo , Feminino , Histonas/metabolismo , Humanos , Masculino , Pessoa de Meia-Idade , Peroxidase/metabolismo , Gravidez , Adulto Jovem
11.
Oncol Rep ; 40(6): 3469-3478, 2018 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-30272334

RESUMO

The present study aimed to examine the role of microRNA­433 in the growth and death of cervical cancer cells. RNA isolation, reverse transcription­quantitative polymerase chain reaction analysis, an MTT assay, flow cytometry, and western blot analysis were used for this investigation. The results showed that the expression of microRNA­433 was downregulated in patients with cervical cancer. The disease­free survival and overall survival rates of patients with low expression levels of microRNA­433 were lower, compared with those in patients with high expression levels of microRNA­433. The expression levels of microRNA­433 were downregulated in cervical cancer in vitro. It was found that the downregulation of microRNA­433 promoted the growth and inhibited the apoptosis of cervical cancer cells through activating focal adhesion kinase (FAK)/phosphoinositide 3­kinase (PI3K)/AKT signaling. However, the upregulation of microRNA­433 induced apoptosis and suppressed the growth of cervical cancer cells through inhibiting the FAK/PI3K/AKT signaling pathway. In addition, FAK or PI3K inhibitors promoted the death of cervical cancer cells following the downregulation of microRNA­433. These results revealed that microRNA­433 suppressed the growth of cervical cancer cells via the FAK/PI3K/AKT signaling pathway.


Assuntos
Regulação para Baixo , Quinase 1 de Adesão Focal/genética , MicroRNAs/genética , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Neoplasias do Colo do Útero/genética , Apoptose , Linhagem Celular Tumoral , Proliferação de Células , Feminino , Quinase 1 de Adesão Focal/metabolismo , Regulação Neoplásica da Expressão Gênica , Humanos , Pessoa de Meia-Idade , Prognóstico , Transdução de Sinais , Análise de Sobrevida , Neoplasias do Colo do Útero/metabolismo
12.
Iran J Public Health ; 47(8): 1090-1097, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-30186780

RESUMO

Background: This study was designed to investigate the clinical effects of different treatment methods on stress urinary incontinence (SUI) in perimenopausal women, and to evaluate urodynamic characteristics. Methods: Seventy-two menopausal female patients with stress urinary incontinence were included in the Second Affiliated Hospital of Soochow University from January 2016 to July 2017. The cases were divided into 3 groups of 24 each, depending on the treatment received. Group A patients received treatment with electrical stimulation combined with biofeedback; those in group B received conventional pelvic floor muscle exercise therapy; and those in group C did not have any treatment. Relevant clinical parameters of urination were determined including pelvic floor muscle strengths, urine dynamics indexes and ICS quality of life survey scores; results were averaged in each group for comparisons among the three groups before and after the 60-day study period. Results: After treatment for 60 days, both group A and B patients displayed a clear improvement in their urinary incontinence, pelvic floor muscle strength, leakage times, frequency of urination, urine dynamics index and ICS scores (P<0.05), with group A showing the most improvement. Women in group C showed no significant difference before and after the 60-day study period (P>0.05). Conclusion: Both the method of electrical stimulation combined with biofeedback, and conventional pelvic floor muscle exercises could help perimenopausal women with stress urinary incontinence; however, electrical stimulation combined with biological feedback seems to bring about better clinical effects.

13.
PLoS One ; 13(2): e0191756, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29401471

RESUMO

CA125 amounts have a large overlap in ovarian cancer and benign diseases. We conducted a retrospective cohort trial to assess the clinical value of circulating cell-free DNA concentration and integrity index for the diagnosis of ovarian cancer. A total of 150 patients were recruited. Plasma samples of 24 ovarian cancer patients, 12 benign ovarian cysts, and 12 healthy controls were assessed. By amplifying short ALU-115 repeat and long ALU-219 fragments, circulating cell-free DNA concentrations and integrity index were measured. Plasma ALU-219 fragment levels and integrity index were significantly higher in the ovarian cancer group compared with the benign disease and healthy control groups (p = 0.023 and p = 0.004, respectively). These findings indicated that plasma ALU-219 levels and integrity may have a clinical value in the early diagnosis of ovarian cancer.


Assuntos
Neoplasias Ovarianas/diagnóstico , Diagnóstico Precoce , Feminino , Humanos , Reação em Cadeia da Polimerase em Tempo Real , Estudos Retrospectivos
14.
Oncotarget ; 8(19): 31386-31394, 2017 May 09.
Artigo em Inglês | MEDLINE | ID: mdl-28404901

RESUMO

It is generally known that the human genome makes a large amount of noncoding RNAs compared with coding genes. Long non-coding RNAs (lncRNAs) which composed of more than 200 nucleotides have been described as the largest subclass of the non-coding transcriptome in human noncoding RNAs. Existing research shows that lncRNAs exerted biological functions in various tumors via participating in both oncogenic and tumor suppressing pathways. The previous studies indicated that lncRNA taurine upregulated 1 (TUG1) play important roles in the initiation and progression of malignancies. In this study,based on previous research, we investigated the expression and biological role of the lncRNA-TUG1. We analyzed the relationship between lncRNA-TUG1and endometrial carcinoma (EC) in a total 104 EC carcinoma specimens, compared with that in normal tissues. We found that lncRNA-TUG1 expression in cancer tissues was significantly higher than that in adjacent tissues. Through a series of experiments, the results demonstrated that lncRNA-TUG1 enhances the evolution and progression of EC through inhibiting miR-299 and miR-34a-5p.


Assuntos
Neoplasias do Endométrio/genética , Regulação Neoplásica da Expressão Gênica , MicroRNAs/genética , Interferência de RNA , RNA Longo não Codificante/genética , Linhagem Celular Tumoral , Proliferação de Células , Transformação Celular Neoplásica/genética , Neoplasias do Endométrio/patologia , Feminino , Técnicas de Silenciamento de Genes , Humanos , Fator A de Crescimento do Endotélio Vascular/genética
15.
Oncol Rep ; 37(1): 155-162, 2017 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-27878291

RESUMO

Cancer stem cells are a small subset of cancer cells that contribute to cancer progression, metastasis, chemoresistance and recurrence. CD133-positive (CD133+) ovarian cancer cells have been identified as ovarian cancer stem cells. Adenovirus-mediated gene therapy is an innovative therapeutic method for cancer treatment. In the present study, we aimed to develop a new gene therapy to specifically eliminate CD133+ ovarian cancer stem cells by targeting CD133. We used the Cre/LoxP system to augment the selective expression of the truncated Bid (tBid) gene as suicide gene therapy in CD133+ ovarian cancer stem cells. The adenovirus (Ad)-CD133-Cre expressing Cre recombinase under the control of the CD133 promoter and Ad-CMV-LoxP-Neo-LoxP-tBid expressing tBid under the control of the CMV promoter were successfully constructed using the Cre/LoxP switching system. The co-infection of Ad-CMV-LoxP-Neo-LoxP-tBid and Ad-CD133-Cre selectively induced tBid overexpression, which inhibited cell growth and triggered the cell apoptosis of CD133+ ovarian cancer stem cells. The Cre/LoxP system-mediated tBid overexpression activated the pro-apoptotic signaling pathway and augmented the cytotoxic effect of cisplatin in CD133+ ovarian cancer stem cells. Furthermore, in xenograft experiments, co-infection with the two recombinant adenoviruses markedly suppressed tumor growth in vivo and promoted cell apoptosis in tumor tissues. Taken together, the present study provides evidence that the adenovirus-mediated tBid overexpression induced by the Cre/LoxP system can effectively eliminate CD133+ ovarian cancer stem cells, representing a novel therapeutic strategy for the treatment of ovarian cancer.


Assuntos
Adenoviridae/genética , Apoptose/genética , Proteína Agonista de Morte Celular de Domínio Interatuante com BH3/genética , Terapia Genética/métodos , Integrases/genética , Células-Tronco Neoplásicas/fisiologia , Neoplasias Ovarianas/terapia , Antígeno AC133/metabolismo , Animais , Proteína Agonista de Morte Celular de Domínio Interatuante com BH3/química , Códon sem Sentido , Feminino , Regulação Neoplásica da Expressão Gênica , Técnicas de Transferência de Genes , Vetores Genéticos , Células HEK293 , Humanos , Camundongos , Camundongos SCID , Mutagênese Sítio-Dirigida , Células-Tronco Neoplásicas/metabolismo , Células-Tronco Neoplásicas/patologia , Neoplasias Ovarianas/genética , Neoplasias Ovarianas/metabolismo , Neoplasias Ovarianas/patologia , Células Tumorais Cultivadas , Ensaios Antitumorais Modelo de Xenoenxerto
16.
Oncol Res ; 25(4): 595-603, 2017 Apr 14.
Artigo em Inglês | MEDLINE | ID: mdl-27760587

RESUMO

Ovarian cancer is one of the most lethal malignant gynecologic tumors with a high relapse rate worldwide. Cancer stem cells (CSCs) have been identified in ovarian cancer and other malignant tumors as a small population of cells that are capable of self-renewal and multidifferentiation. CD133+ ovarian CSCs have been reported to be more tumorigenic and more resistant to chemotherapeutic treatment. Thus, CD133 has emerged as one of the most promising therapeutic markers for ovarian cancer treatment. In the current study, we constructed a recombinant adenovirus Cre/loxP regulation system to selectively introduce truncated Bid (tBid) expression specifically targeting CD133+ in ovarian CSCs. The results demonstrated that the coinfection of Ad-CD133-Cre and Ad-CMV-LoxP-Neo-LoxP-tBid significantly increased tBid expression in CD133+ ovarian CSCs. Moreover, the tBid overexpression induced by a recombinant adenovirus Cre/loxP system dramatically inhibited cell proliferation and invasion, significantly elevated cell apoptosis, and activated the mitochondrial apoptosis pathway in CD133+ ovarian CSCs. Additionally, recombinant adenovirus Cre/loxP system-mediated tBid overexpression suppressed the tumorigenic potential of CD133+ ovarian CSCs in a xenograft mouse model. In conclusion, our study successfully constructed a recombinant adenovirus Cre/loxP system and induced tBid overexpression in CD133+ ovarian CSCs, providing a new therapeutic approach for ovarian cancer treatment.


Assuntos
Antígeno AC133/metabolismo , Proteína Agonista de Morte Celular de Domínio Interatuante com BH3/genética , Transformação Celular Neoplásica/genética , Células-Tronco Neoplásicas/metabolismo , Neoplasias Ovarianas/genética , Neoplasias Ovarianas/metabolismo , Adenoviridae/genética , Animais , Apoptose/genética , Linhagem Celular Tumoral , Proliferação de Células , Modelos Animais de Doenças , Feminino , Expressão Gênica , Regulação Neoplásica da Expressão Gênica , Vetores Genéticos/genética , Recombinação Homóloga , Humanos , Camundongos , Mitocôndrias/genética , Mitocôndrias/metabolismo , Neoplasias Ovarianas/patologia , Deleção de Sequência , Transdução Genética , Ensaios Antitumorais Modelo de Xenoenxerto
17.
Oncol Lett ; 14(6): 7225-7231, 2017 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-29344157

RESUMO

The programmed death-1 (PD-1) signaling pathway serves a critical role in immune regulation and tolerance by suppressing the activation and proliferation of T cells. The aim of the present study was to investigate the effect of PD-1 and programmed death-ligand 1 (PD-L1) on the development of cervical carcinoma and cervical intraepithelial neoplasia (CIN). A total of 40 healthy controls (HC), 40 patients with CIN and 66 newly diagnosed cervical cancer patients were recruited. The expression level of PD-1 expression on peripheral cluster of differentiation (CD)4+ and CD8+ T cells and PD-L1 on monocytes was analyzed by flow cytometry. The expression level of soluble PD-L1 in serum was determined by an ELISA. The results of the present study demonstrated that the PD-1 expression level on CD4+ and CD8+ T cells was significantly increased in CIN and cervical cancer, compared with that in HC. In addition, the PD-1 expression level on CD4+ and CD8+ T cells was increased in cervical cancer, compared with that in CIN. However, the expression level of PDL-1 on CD14+ monocytes was increased in cancer and CIN, but limited in cancer and CIN. In addition, PD-1 expression on CD4+ T cells was positively associated with PD-1 expression on CD8+ T cells in cervical cancer (P<0.05). Further analyses revealed that the proportion of PD-1 on CD4+ and CD8+ T cells were positively associated with tumor stages. However, no difference in the degree of soluble PD-1 among cancer, CIN and HC cells was revealed. The results suggested that the PD-1 signaling pathway is involved in the development of CIN and cervical cancer.

18.
Oncol Lett ; 9(5): 2090-2094, 2015 May.
Artigo em Inglês | MEDLINE | ID: mdl-26137018

RESUMO

The purpose of the present study was to investigate the expression of TAp73 and ΔNp73 in cervical squamous cancer cells, and to evaluate the prognostic significance of TAp73 and ΔNp73 expression in patients with International Federation of Gynecology and Obstetrics (FIGO) stage I-II cervical squamous cell carcinoma (SCC). The immunohistochemical expression of TAp73 and ΔNp73 was evaluated in 59 FIGO stage I-II cervical SCC tumor samples. Correlations with clinicopathological characteristics were determined by χ2 test. The prognostic impact of TAp73 and ΔNp73 expression with regard to overall survival (OS) was determined by the Kaplan-Meier method. High TAp73 and ΔNp73 expression was detected in 79.7% (47/59) and 76.3% (45/59) of patients, respectively. The expression of TAp73 and ΔNp73 was not associated with age, FIGO stage, pathological differentiation or lymph node metastasis. The 3-year OS rates associated with low and high TAp73 expression were 75.0 and 83.0%, respectively (χ2=0.33; P=0.568), whereas those associated with low and high ΔNp73 expression were 100.0 and 75.6%, respectively (χ2=3.90; P=0.048). High expression levels of TAp73 and ΔNp73 were frequently observed in the cervical squamous cancer cells. Overall, high expression levels of ΔNp73 may indicate an unfavorable prognosis in patients with early-stage cervical SCC.

19.
Biomed Pharmacother ; 73: 129-34, 2015 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-26211593

RESUMO

BACKGROUND AND PURPOSES: Through reducing immune response, VTCN1 could promote carcinoma indirectly. However, the direct effect of VTCN1 on carcinoma was not studied clearly, especially on ovarian carcinoma. In this paper, we verified the potential effect and mechanism of VTCN1 on ovarian carcinoma. METHODS: The influence of high or low VTCN1 expression on the viability of ovarian cancer was detected by CKK-8 and annexin V-PI kit. The orthotopicxenograft tumor model was performed to evaluate the effect of VTCN1 on the promotion of tumor in vivo. Western blot was used to verify the signaling pathways predicted by bioinformatics analysis. RESULTS: Low expression of VTCN1 could inhibit the viability and metastasis of ovarian carcinoma directly in vitro and vivo; Information analysis demonstrated that cell cycle and JAK2/STAT were involved in the regulation of VTCN1. The CDK2/4 and CDC25C expression and phosphorylation of JAK2/STAT had a direct relationship with the reduction of VTCN1. CONCLUSIONS: VTCN1 could affect the viability and metastasis of ovarian carcinoma by reducing the expression of CDK2/4 and CDC25C and phosphorylation of JAK2/STAT. It indicated that VTCN1 was a potential target for treating ovarian carcinoma.


Assuntos
Progressão da Doença , Neoplasias Ovarianas/metabolismo , Neoplasias Ovarianas/patologia , Inibidor 1 da Ativação de Células T com Domínio V-Set/biossíntese , Animais , Linhagem Celular Tumoral , Proliferação de Células/fisiologia , Sobrevivência Celular/fisiologia , Feminino , Humanos , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Ensaios Antitumorais Modelo de Xenoenxerto/métodos
20.
Int J Clin Exp Pathol ; 8(10): 13261-6, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-26722527

RESUMO

BACKGROUND: Dysregulation of long non-coding RNAs (lncRNAs) plays critical roles in tumor progression. The purpose of this study was to investigate the relationship between lncRNA CCAT2 expression and cervical squamous cell cancer susceptibility and prognosis. METHODS: Expression levels of lncRNA CCAT2 in 123 cervical squamous cell tumor specimens were determined by quantitative real-time PCR (qRT-PCR), to clarify the clinical significance of lncRNA CCAT2 in cervical squamous cell cancer, we further discussed the relationship between lncRNA CCAT2 expression and overall survival (OS) and progression-free survival (PFS). RESULTS: In the present study, we found that lncRNA CCAT2 was up-regulated in cervical squamous cell cancer tissues compared to the adjacent non-tumor tissues. In addition, the high lncRNA CCAT2 expression was significantly associated with the FIGO stage, lymph node metastasis and depth of cervical invasion (P<0.05). Furthermore, patients with high expression of lncRNA CCAT2 had poor OS (HR=2.813, 95% CI: 1.504-6.172; P=0.017), and PFS rates (HR=3.072, 95% CI: 1.716-8.174; P=0.008). Multivariate Cox proportional hazard model analysis demonstrated that high lncRNA CCAT2 expression was an independent poor prognostic factor for cervical squamous cell cancer patients. CONCLUSIONS: Our study suggested that high expression of lncRNA CCAT2 is related to the prognosis of cervical squamous cell cancer; it may be a new prognostic biomarker and potential therapeutic target for cervical squamous cell cancer intervention.


Assuntos
Carcinoma de Células Escamosas/genética , Metástase Neoplásica/genética , RNA Longo não Codificante/genética , Regulação para Cima , Neoplasias do Colo do Útero/genética , Adulto , Carcinoma de Células Escamosas/metabolismo , Carcinoma de Células Escamosas/mortalidade , Carcinoma de Células Escamosas/patologia , Progressão da Doença , Feminino , Humanos , Pessoa de Meia-Idade , Metástase Neoplásica/patologia , Estadiamento de Neoplasias , Prognóstico , RNA Longo não Codificante/metabolismo , Taxa de Sobrevida , Neoplasias do Colo do Útero/metabolismo , Neoplasias do Colo do Útero/mortalidade , Neoplasias do Colo do Útero/patologia
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