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1.
J Cell Biochem ; 121(2): 1823-1833, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31680313

RESUMO

Glioma with poor prognosis is accepted as a lethal, malignant intracranial tumor among central nervous system diseases. It has been frequently exhibited that long noncoding RNAs (lncRNAs) exert indispensable functions in glioma through regulating gene expression through various molecular mechanisms. To unveil a novel lncRNA functioning in glioma, we browsed the cancer genome atlas dataset and chose the lncRNA PC-esterase domain containing 1B antisense RNA 1 (PCED1B-AS1) for further investigations. Loss-of-function experiments depicted that the proliferation ability was restrained and apoptosis ability was induced in glioma cells by PCED1B-AS1 silencing and this phenomenon was also observed when PCED1B was knocked down. In view of the position of PCED1B-AS1 in the cytoplasm, we produced the Venn diagram and discovered one shared microRNA of PCED1B-AS1 and PCED1B. The competing endogenous RNA network formed by PCED1B-AS1, miR-194-5p, and PCED1B was attested by mechanism assays. Rescue experiments reconfirmed that miR-194-5p suppression or PCED1B overexpression neutralized the obstructive impacts of PCED1B-AS1 silence on proliferation and the promoting effects of PCED1B-AS1 silence on apoptosis. The modulation mechanism of the PCED1B-AS1/miR-194-5p/PCED1B axis in glioma was investigated and affirmed, which supports researchers with a new insight into the therapy of patients with glioma.

2.
Cell Oncol (Dordr) ; 2019 Dec 28.
Artigo em Inglês | MEDLINE | ID: mdl-31884576

RESUMO

PURPOSE: The etiology of nasopharyngeal carcinoma (NPC) is multifactorial, complex and not fully characterized yet. MicroRNAs (miRNAs or miRs) have been found to contribute to the development and progression of NPC. Here, we aimed to investigate the putative role of miR-129-5p in NPC lymphangiogenesis and lymph node metastasis (LNM), including the involvement of its target gene ZIC2 and the Hedgehog signaling pathway. METHODS: The expression of miR-129-5p and ZIC2 in primary NPC tissues was assessed using RT-qPCR and Western blot analyses, followed by LNM and lymph vessel density (LVD) correlation analyses. A direct interaction between miR-129-5p and ZIC2 was verified using a dual-luciferase reporter assay. Gain- and loss-of-function experiments were conducted to investigate the effects of miR-129-5p and ZIC2 expression on NPC cell invasion, migration and proliferation in vitro, as well as on LDV and LNM in nude mice in vivo. Additionally, RT-qPCR and Western blot analyses were performed to determine the expression levels of Hedgehog signaling pathway-related factors. RESULTS: We found that ZIC2 was highly expressed, and miR-129-5p was lowly expressed, in primary NPC tissues. In addition, we found that miR-129-5p can directly bind to and reduce ZIC2 expression. LVD was found to be negatively correlated with miR-129-5p and to be positively correlated with ZIC2 expression. Concomitantly, we found that miR-129-5p abrogated activation of the Hedgehog signaling pathway via ZIC2 targeting, leading to suppression of NPC cell invasion, migration and proliferation in vitro as well as suppression of LNM and LVD in vivo. CONCLUSIONS: From our data we conclude that miR-129-5p, by decreasing ZIC2 expression, may inhibit NPC lymphangiogenesis and LNM through suppression of the Hedgehog signaling pathway.

3.
Cell Commun Signal ; 17(1): 173, 2019 Dec 27.
Artigo em Inglês | MEDLINE | ID: mdl-31881947

RESUMO

BACKGROUND: Accumulation of immunosuppressive protein programmed death-ligand 1 (PD-L1) has been documented in several cancers and contributes to the evasion of the host immune system. However, cancer cell-intrinsic signaling-dependent control of PD-L1 expression remains to be elucidated. Herein, we aimed to identify the let-7 family of microRNAs as candidates that up-regulate tumor cell PD-L1 expression and mediates immune evasion of head and neck squamous cell carcinoma (HNSCC). METHODS: The expression of let-7 family and PD-L1 was quantified in HNSCC tissues and adjacent normal tissues. PD-L1 degradation was evaluated in HNSCC cells in response to elevated expressions of let-7a or let-7b. The regulation of let-7 family on PD-L1 degradation through a mechanism involving T-cell factor-4 (TCF-4) control of ß-catenin/STT3 pathway was evaluated. Immune recognition of HNSCC in vivo was examined in subcutaneous tumor-bearing C3H mice in the presence of let-7a/b and/or CTLA-4 antibody. RESULTS: The let-7 family were significantly down-regulated in the context of HNSCC, sharing a negative correlation with PD-L1 expression. Glycosylated PD-L1 was detected in HNSCC cells, which was reduced by let-7a/b over-expression. TCF-4, the target of let-7a/b, activated the ß-catenin/STT3 pathway and promoted PD-L1 degradation. In vivo analysis demonstrated that let-7a/b over-expression potentiated anticancer immunotherapy by CTLA-4 blockade. CONCLUSIONS: Taken together, our findings highlight targeting let-7 family as a potential strategy to enhance immune checkpoint therapy for HNSCC.

4.
Int Immunopharmacol ; 76: 105886, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31520990

RESUMO

α-Cyperone is the volatile oil component in Cyperus rotundus L. The previous reports had shown the inhibition of α-Cyperone on NF-κB signaling in LPS-stimulated RAW264.7 cells. However, it is still unclear whether α-Cyperone could suppress inflammatory response in acute lung injury (ALI) induced by LPS. The aim of this study is to investigate the suppression of α-Cyperone on LPS-induced ALI in mice. In this study, we established the LPS-induced ALI model and compared different doses of α-Cyperone with the control group and LPS group. Accordingly, the following indexes would be compared, including lung wet/dry ratio, MPO activity, inflammatory cell number, histopathological changes, levels of inflammatory cytokines, NF-κB and NLRP3 signaling pathways activation. The results demonstrated that α-Cyperone had the effect on reducing the wet/dry ratio and MPO activity. Furthermore, the increase of inflammatory cells and inflammatory cytokines could be inhibited by α-Cyperone. Meanwhile, α-Cyperone could downregulate NF-κB and NLRP3 signaling pathways. Finally, we found α-Cyperone could up-regulate the expression of SIRT1 and SIRT1 inhibitor could reverse the protective effects of α-Cyperone on ALI. In conclusion, α-Cyperone showed the protective effect on LPS-induced ALI in mice by suppressing the NF-κB and NLRP3 signaling pathways, mainly via up-regulating SIRT1. This provides a potential drug for the treatment of LPS-induced ALI.

5.
Microb Pathog ; 137: 103720, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31494302

RESUMO

Endometritis, a common inflammation of the uterus, often causes severe damage to human and animal reproductive health. Polydatin is a polyphenol extracted from the rhizome of Polygonum cuspidatum that has anti-inflammatory and anti-oxidative effects. The purpose of this study was to investigate the underlying protective effects and mechanisms of polydatin against lipopolysaccharide (LPS)-induced endometritis in mice. The mouse model of endometritis was established by injection of LPS through the vagina. The uterine tissues of each group were gathered to analyze histopathological changes, inflammatory cytokine production, and the degree of activation of the NF-κB and Nrf2 signaling pathways. The myeloperoxidase (MPO) activity assay indicated that polydatin treatment significantly alleviated inflammatory cell infiltration in LPS-induced endometritis mice. Furthermore, polydatin treatment remarkably impeded the expression of TNF-α, IL-1ß, and IL-6 by ELISA assay. Hematoxylin-eosin staining (H&E) showed that polydatin significantly decreased impairment of the uterus. In addition, polydatin was also found to suppress LPS-induced NF-κB activation in a dose-dependent manner. The expression of Nrf2 and HO-1 was enhanced by polydatin treatment. All the results suggest that polydatin helpfully alleviates LPS-induced endometritis by suppressing the NF-ĸB signaling pathway and activating the Nrf2 signaling pathway.

6.
J Cell Biochem ; 120(6): 10830-10846, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30706537

RESUMO

Papillary thyroid carcinoma (PTC) is the most common type of thyroid malignancy, with growing incidence every year. microRNAs (miRs) are known to regulate the physiological and pathological processes of cancers, such as proliferation, migration, invasion, survival, and epithelial-mesenchymal transition (EMT). Herein, this study aimed to investigate the effect of miR-539 on cell proliferation, apoptosis, and EMT by targeting secretory leukocyte protease inhibitor (SLPI) via the transforming growth factor ß1 (TGF-ß1)/Smads signaling pathway in PTC. First, PTC-related differentially expressed genes and regulatory miR were screened using bioinformatics analysis, dual luciferase reporter gene assay, and ribonucleoprotein immunoprecipitation, which identified the SLPI gene and the regulatory miR-539 for this study. We identified SLPI as a highly expressed gene in PTC tissues, and SLPI was targeted and negatively regulated by miR-539. Then, we introduced a series of miR-539 mimics, miR-539 inhibitors, and small interfering RNA against SLPI plasmids into CGTHW-3 cells to examine the effects of miR-539 and SLPI on the expression of TGF-ß1/Smads signaling pathway-, EMT-, and apoptosis-related factors, as well as cell proliferation, migration, invasion, and apoptosis. The obtained results indicated that CGTHW-3 cells treated with silenced SLPI or overexpressed miR-539 suppressed the cell proliferation, migration, invasion abilities, and resistance to apoptosis of PTC cells, corresponding to increased expression of Bcl-2-associated X protein, TGF-ß1, Sekelsky mothers against dpp 4, and epithelial cadherin, and decreased B cell lymphoma 2, Vimentin, and N-cadherin. Altogether, we concluded that overexpressed miR-539 could inhibit the PTC cell proliferation and promote apoptosis and EMT by targeting SPLI via activation of the TGF-ß1/Smads signaling pathway.

7.
Front Pharmacol ; 9: 1001, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30294270

RESUMO

Chronic obstructive pulmonary disease (COPD) is the major leading cause of disease with high-mortality worldwide. Cigarette smoke (CS) is a major factor for COPD. CS causes chronic inflammation and oxidative stress, which contributes to lung dysfunction in COPD. Isoliquiritigenin (ILG), a natural flavonoid derived from the root of liquorice, has been reported to possess antiinflammatory and antioxidant activity. In the present study, we tested the mechanism and protective effects of ILG on CS-induced COPD. Mice were exposed to CS for 2 h twice a day for 4 weeks. ILG was given orally 1 h before CS exposure twice a day for 4 weeks. The bronchial alveolar lavage fluid was collected to test the levels of inflammatory cytokines and the number of inflammatory cells. The lung tissues were obtained to evaluate the pathological changes, lung edema, myeloperoxidase (MPO) activity, malondialdehyde (MDA) level, as well as the expression of the nuclear factor-erythroid 2 (Nrf2) and nuclear factor κB (NF-κB) signaling pathways. The results showed that ILG reduced the infiltration of inflammatory cells and the production of inflammatory cytokines. ILG also reversed CS-induced lung pathological injuries, wet/dry ratio, MPO activity, and MDA level. Further research also showed that ILG dose-dependently up-regulated the expression of Nrf2 and down-regulated the expression of NF-κB signaling pathways induced by CS. In conclusion, ILG protected against CS-induced COPD by inhibiting inflammatory and oxidative stress via the regulation of the Nrf2 and NF-κB signaling pathways.

8.
Int Arch Allergy Immunol ; 170(3): 180-6, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27576536

RESUMO

BACKGROUND: Sappanone A (SA) is isolated from the heartwood of Caesalpinia sappan and exerts a wide range of pharmacological activities. In the present study, we investigated the protective effects of SA on allergic asthma in a murine model of ovalbumin (OVA)-induced asthma. METHODS: BALB/c mice were sensitized and challenged. Then, the mice were intraperitoneally injected with SA (12.5, 25 and 50 mg/kg) 1 h before OVA challenge; 24 h after the last challenge, the mice were sacrificed, and data were collected by different experimental methods. RESULTS: The results showed that SA dose-dependently reduced inflammatory cell counts, levels of cytokines IL-4, IL-5 and IL-13, and OVA-specific IgE in bronchoalveolar lavage fluid. The level of IFN-γ decreased by OVA was upregulated by the treatment with SA. Furthermore, SA was found to attenuate the airway inflammation and mucus hypersecretion induced by the OVA challenge. In addition, SA dose-dependently upregulated the expression of Nrf2 and HO-1. SA inhibited OVA-induced asthma by activating the Nrf2 signaling pathway. CONCLUSIONS: These data suggest that SA may have a potential use as a therapeutic agent for asthma.


Assuntos
Asma/imunologia , Asma/patologia , Isoflavonas/farmacologia , Ovalbumina/imunologia , Animais , Asma/tratamento farmacológico , Asma/metabolismo , Líquido da Lavagem Broncoalveolar/citologia , Líquido da Lavagem Broncoalveolar/imunologia , Citocinas/metabolismo , Modelos Animais de Doenças , Feminino , Imunoglobulina E/sangue , Imunoglobulina E/imunologia , Leucócitos/imunologia , Leucócitos/metabolismo , Linfócitos/imunologia , Linfócitos/metabolismo , Camundongos , Fator 2 Relacionado a NF-E2/metabolismo , Ovalbumina/efeitos adversos , Transdução de Sinais
9.
Int Immunopharmacol ; 38: 324-31, 2016 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-27344638

RESUMO

Biochanin A, an isoflavone existed in red clover and peanuts, has been reported to possess a wide spectrum of pharmacological activities, such as anti-inflammatory and antioxidant effects. However, the protective effects and mechanism of biochanin A on liver injury have not been reported. In this study, acute liver injury was induced by intraperitoneal injection of lipopolysaccharide (LPS) and d-galactosamine (D-GalN). Biochanin A was administrated 1h prior to LPS/D-GalN challenge. Serum ALT, AST, IL-1ß, and TNF-α levels, hepatic malondialdehyde (MDA), GPx, SOD, and Catalase contents, tissue histology, IL-1ß, TNF-α, NLRP3, and Nrf2 expression were detected. The results showed that serum ALT, AST, IL-1ß, and TNF-α levels and hepatic MDA content increased after LPS/GalN treatment. These changes were attenuated by biochanin A. Meanwhile, biochanin A dose-dependently up-regulated the expression of Nrf2 and HO-1. Biochanin A also inhibited hepatic IL-1ß and TNF-α expression in a dose-dependent manner. Biochanin A did not inhibit LPS/D-GalN-induced hepatic NLRP3, ASC, and caspase-1 expression. However, the interaction of NLRP3 with ASC and caspase-1 were inhibited by biochanin A. In addition, LPS/D-GalN-induced up-regulation of thioredoxin-interacting protein (TXNIP) and interaction between TXNIP and NLRP3 were also inhibited by biochanin A. In conclusion, biochanin A protected against LPS/GalN-induced liver injury by activating the Nrf2 pathway and inhibiting NLRP3 inflammasome activation.


Assuntos
Anti-Inflamatórios/uso terapêutico , Doença Hepática Induzida por Substâncias e Drogas/tratamento farmacológico , Genisteína/uso terapêutico , Inflamassomos/efeitos dos fármacos , Fígado/efeitos dos fármacos , Animais , Proteínas de Transporte/genética , Proteínas de Transporte/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/imunologia , Galactosamina/imunologia , Heme Oxigenase-1/genética , Heme Oxigenase-1/metabolismo , Inflamassomos/metabolismo , Interleucina-1beta/metabolismo , Lipopolissacarídeos/imunologia , Fígado/metabolismo , Fígado/patologia , Masculino , Proteínas de Membrana/genética , Proteínas de Membrana/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Fator 2 Relacionado a NF-E2/genética , Fator 2 Relacionado a NF-E2/metabolismo , Proteína 3 que Contém Domínio de Pirina da Família NLR/genética , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Transdução de Sinais/efeitos dos fármacos , Tiorredoxinas/genética , Tiorredoxinas/metabolismo , Fator de Necrose Tumoral alfa/metabolismo
10.
Tumour Biol ; 37(2): 2209-17, 2016 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-26353857

RESUMO

Mesoporous silica nanoparticles (MSNs) represent a new form of drug nanocarrier with thermo/pH-coupling sensitivity and site-specificity. CD133(+) Hep-2 laryngeal cancer cells are responsible for multidrug resistance due to elevated expression of ABCG2. Since positively charged nanoparticles could easily uptake nucleic acids, we examined the possibility of using this new drug delivery system to simultaneously deliver different chemotherapeutic drugs and siRNA targeting ABCG2. Our results demonstrated that both antitumor drugs and siRNA against ABCG2 were successfully delivered into CD133(+) cancer cells by loaded MSNs. Down-regulation of ABCG2 significantly enhanced the efficacy of chemotherapeutic drug-induced apoptosis in laryngeal carcinoma cells. Furthermore, the chemotherapeutic drug and siRNA loaded nanoparticles inhibited tumor growth in vivo in a laryngeal cancer mouse model.


Assuntos
Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/antagonistas & inibidores , Sistemas de Liberação de Medicamentos/métodos , Neoplasias Laríngeas , Nanopartículas , Proteínas de Neoplasias/antagonistas & inibidores , RNA Interferente Pequeno/genética , Antígeno AC133/metabolismo , Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP/genética , Animais , Antineoplásicos/farmacologia , Western Blotting , Linhagem Celular Tumoral , Portadores de Fármacos/farmacologia , Resistência a Múltiplos Medicamentos/genética , Resistencia a Medicamentos Antineoplásicos/genética , Feminino , Citometria de Fluxo , Técnicas de Silenciamento de Genes/métodos , Humanos , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Proteínas de Neoplasias/genética , Dióxido de Silício
11.
Cell Biochem Biophys ; 71(1): 261-9, 2015 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-25241082

RESUMO

The objective of this study is to investigate the chemoresistance of CD133(+) cancer stem cells in Hep-2 cells of laryngeal cancer and detect the expression mRNA and protein levels of BMI-1 in CD133(+) cells and CD133(-) cells. The response of Hep-2 cells to different chemotherapeutic agents was investigated, and the expression of CD133 was studied. Fluorescence-activated cell sorting analysis was used to identify CD133, and the CD133(+) subset of cells was separated and analyzed chemotherapy resistance. Colony formation assays were studied and cells were injected subcutaneously into axillary fossa of node mice to measure the tumor-forming ability. RT-PCR and Western blot analyses were used to detect the expression levels of BMI-1 in the different subpopulation cells. It was concluded that chemotherapy enriched the CD133(+) subpopulation 2-fourfold, relative to the untreated cells. 1.55 ± 0.28% of Hep-2 cells were observed to be CD133(+) cells. Flow cytometric analysis revealed that after the treatment with these chemotherapeutic agents, the expression of CD133 was up to 5.16 ± 0.86%, 4.94 ± 0.58%, 3.66 ± 0.59%. After 5-FU treatment, the expression of CD133 was 6.7 ± 1.6% relative to the untreated mice 2.6 ± 0.96% by nude mice tumor xenograft model. CD133(+) cancer stem cells were more resistant to chemotherapy; the proliferation capability and tumor-forming ability were no difference after chemotherapy. Semi-quantitative RT-PCR and Western blot analyses provided strong evidence that BMI-1 expression in CD133(+) cells is different from CD133(-) cells remarkably. Taken together, it was confirmed that CD133(+) cancer stem cells were chemoresistant and BMI-1 was highly expressed in these CD133(+) cells.


Assuntos
Neoplasias Laríngeas/patologia , Células-Tronco Neoplásicas/metabolismo , Complexo Repressor Polycomb 1/metabolismo , Antígeno AC133 , Animais , Antígenos CD/metabolismo , Carboplatina/farmacologia , Carcinogênese/efeitos dos fármacos , Linhagem Celular Tumoral , Docetaxel , Resistencia a Medicamentos Antineoplásicos , Fluoruracila/farmacologia , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Glicoproteínas/metabolismo , Humanos , Camundongos , Células-Tronco Neoplásicas/efeitos dos fármacos , Células-Tronco Neoplásicas/patologia , Peptídeos/metabolismo , Complexo Repressor Polycomb 1/genética , Taxoides/farmacologia
12.
Asian Pac J Trop Med ; 7(11): 867-72, 2014 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-25441985

RESUMO

OBJECTIVE: To explore the inhibitive and apoptosis inductive effect of IL-24 genes on CD133(+) laryngeal cancer cells in Hep-2 line. METHODS: Human peripheral blood monocytes were isolated. The total RNA was extracted by using Trizol method and reverse transcripted into cDNA using RT-PCR method. Primers P1 and P2 was designed for the amplification of human IL-24 genes. After confirmation of agarose gel electrophoresis tests, TA was cloned into pMD19-T simple vector. Nhe I and Xho I double digesting human IL-24 and pIRES2-ZsGreen1 and eukaryotic expression vector were used to establish the pIRES2-ZsGreen1-hIL-24 vector, and detected by enzyme digestion and gene sequencing methods. Flow cytometry (FCM) was used to isolate CD133(+) cells from Hep-2 cells. CD133(+) cells were transfected with pIRES2-ZsGreen1-hIL-24 through liposome 2000. After detection, MTT and FCM were used to observe the effect of IL-24 gene on CD133(+) laryngeal cancer Hep-2 cells. RESULTS: Lipotin mediated transfection of recombinant pIRES2-ZsGreen1-hIL-24 plasmid into CD133(+) Hep-2 could expressed IL-24 gene in cells stably. MTT results showed that IL-24 transfected group was significantly suppressed compared to empty vector group and control group (P<0.05); FCM results showed that the apoptosis rate of experimental group increased significantly compared to empty vector group and control group (P<0.05). CONCLUSIONS: IL-24 gene expressions can inhibit proliferation of CD133(+) laryngeal cells in Hep-2 line and promote their apoptosis.

13.
Int J Clin Exp Med ; 7(10): 3305-12, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-25419362

RESUMO

Endoscopy is essential for the diagnosis and treatment of cancers derived from the larynx. However, a laryngoscope with conventional white light (CWL) has technical limitations in detecting small or superficial lesions on the mucosa. Narrow band imaging especially combined with magnifying endoscopy (ME) is useful for the detection of superficial squamous cell carcinoma (SCC) within the oropharynx, hypopharynx, and oral cavity. A total of 3675 patients who have come to the outpatient clinic and complained of inspiratory stridor, dyspnea, phonation problems or foreign body sensation, were enrolled in this study. We describe the glottic conditions of the patients. All 3675 patients underwent laryngoscopy equipped with conventional white light (CWL) and NBI system. 1149 patients received a biopsy process. And 1153 lesions were classified into different groups according to their histopathological results. Among all the 1149 patients, 346 patients (312 males, 34 females; mean age 62.2±10.5 years) were suspected of having a total of 347 precancerous or cancerous (T1 or T2 without lymphnode involvement) lesions of the larynx under the CWL. Thus, we expected to attain a complete vision of what laryngeal lesions look like under the NBI view of a laryngoscope. The aim was to develop a complete description list of each laryngeal conditions (e.g. polyps, papilloma, leukoplakia, etc.), which can serve as a criteria for further laryngoscopic examinations and diagnosis.

14.
Tumour Biol ; 34(6): 3603-10, 2013 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-23807678

RESUMO

In this study, we try to detect and isolate the cancer stem cell-like side population cells (SP) from the laryngeal carcinoma cell line and primary laryngeal carcinoma and explore the clinical implications of SP cells in laryngeal carcinoma. The SP cells and non-side population cells (NSP) cells were sorted by Hoechst 33342 through FACS. The proliferation capacity, invasion ability, migration ability, and tumorigenic activity of the SP cells were evaluated. In addition, the association between the SP cells ratio and the prognostic factors of laryngeal cancer was analyzed. As a result, the percentage of the SP cells in Hep-2 cells was 5.1%. The SP cells depicted float colonies, but the NSP cells failed to generate the typical cell spheres. The clone formation ratios were 47.47 ± 10.20% vs. 4.98 ± 1.41% in the flat plates and 46.82 ± 5.67% vs. 12.53 ± 3.51% in the soft agar for SP and NSP cells (P = 0.01 and 0.01). The SP cells depicted a higher migrating potency than the NSP cells in both the transwell assay and scarification test (all P < 0.05). The matrigel invasion assay showed that the artificial basement membrane penetration rate of SP cells was 39.04 ± 4.78%, which was higher than 25.16 ± 4.63% of the NSP cells (P < 0.05). Only 10(3) SP cells were able to form tumors in mice, whereas 10(4) NSP cells failed to form tumors. The SP cells were correlated with the differentiation, lymph node metastasis, and clinical stage of the laryngeal cancers. In conclusion, SP cells may be a potential prognostic factor of laryngeal cancer.


Assuntos
Neoplasias Laríngeas/patologia , Células-Tronco Neoplásicas/patologia , Células da Side Population/patologia , Esferoides Celulares/patologia , Membro 2 da Subfamília G de Transportadores de Cassetes de Ligação de ATP , Transportadores de Cassetes de Ligação de ATP/genética , Transportadores de Cassetes de Ligação de ATP/metabolismo , Animais , Western Blotting , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , Separação Celular/métodos , Transformação Celular Neoplásica/genética , Transformação Celular Neoplásica/metabolismo , Transformação Celular Neoplásica/patologia , Citometria de Fluxo , Humanos , Neoplasias Laríngeas/genética , Neoplasias Laríngeas/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Microscopia de Fluorescência , Proteínas de Neoplasias/genética , Proteínas de Neoplasias/metabolismo , Células-Tronco Neoplásicas/metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Células da Side Population/metabolismo , Esferoides Celulares/metabolismo , Transplante Heterólogo , Células Tumorais Cultivadas
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