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BACKGROUND: A significant challenge in cancer therapy is to maximize the therapeutic efficacy and minimize the side effects. In the past decade, a lot of nanoparticles have been used as the carriers for efficient drug delivery. METHODS AND RESULTS: This study was to prepare R9 modified with 125I-labeled cRGD and ce6 which self-assembled with miR-139-5p to form nanoparticles (Ce6-R9-125I-RGD-MNPs), and to further take advantage of the enhanced permeability and retention (EPR) effect of radiolabeled nanoparticles to realize the integration of tumor diagnosis and treatment. We successfully synthesized and represented it, saline and serum stability experiments demonstrating good stability. Moreover, Ce6-R9-125I-RGD-MNPs showed superior tumor targeting and the effect of combined photodynamic therapy (PDT) and radiotherapy treatment in vivo and vitro. CONCLUSION: The pathological results further confirmed that the therapeutic doses of Ce6-R9-125I-RGD-MNPs cause pathological changes of tumor tissues while showing minimal toxicity to normal tissues.
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Antineoplásicos/farmacología , Sistemas de Liberación de Medicamentos , MicroARNs/química , Neoplasias/terapia , Péptidos/farmacología , Fotoquimioterapia , Fármacos Fotosensibilizantes/farmacología , Antineoplásicos/síntesis química , Antineoplásicos/química , Relación Dosis-Respuesta a Droga , Humanos , Radioisótopos de Yodo , Estructura Molecular , Nanopartículas/química , Péptidos/síntesis química , Péptidos/química , Procesos Fotoquímicos , Fármacos Fotosensibilizantes/síntesis química , Fármacos Fotosensibilizantes/química , Relación Estructura-ActividadRESUMEN
BACKGROUND: To improve the prognosis outcome of lung cancer patients, more investigations are still needed. Previous reports have demonstrated the function of Ferulic Acid (FA) in lung cancer; thus, we have attempted to probe more molecular mechanisms underlying FA application in lung cancer. METHODS: CCK8 and colony formation experiments have been employed to explore cell viability and proliferation. Cell apoptosis was evaluated through flow cytometry. Cell morphology was observed with a microscope. MMP was assessed by JC-1 and LDH activity was evaluated by relative kit. Western blot assays were performed to examine the expression levels of GSDMD, GSDMD-N, caspase family proteins, and ROS/JNK/Bax mitochondrial apoptosis pathway downstream proteins. Flow cytometry analysis also measured the level of ROS. Tissues from animal models were taken for IHC analysis of C-caspase-1. RESULTS: FA was found to inhibit proliferation, change cell morphology, decrease MMP, and enhance LDH activity, suggesting its ability to induce pyroptosis of lung cancer cells. Both caspase-1 and GSDMD were found to be involved in the pyroptosis of lung cancer cells treated with FA, and caspase-1 mediated GSDMD. Moreover, FA was validated to regulate pyroptosis by ROS/JNK/Bax mitochondrial apoptosis pathway in vitro and in vivo. CONCLUSION: In summary, FA regulates GSDMD through ROS/JNK/Bax mitochondrial apoptosis pathway to induce pyroptosis in lung cancer cells, which may offer a theoretical basis for pyroptosis in the occurrence of lung cancer.
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Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the control data in Fig. 2B and C on p. 7332, showing immunofluorescence and migration assay experiments respectively, were strikingly similar to data appearing in different form in another article which was written by different authors at different research institutes [Tian L, Shen D, Li X, Shan X, Wang X, Yan Q and Liu J: Ginsenoside Rg3 inhibits epithelialmesenchymal transition (EMT) and invasion of lung cancer by downregulating FUT4. Oncotarget 7: 16191632, 2016]. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 16: 73297336, 2017; DOI: 10.3892/mmr.2017.7517].
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The droplet microfluidic device has become a widely used tool in fields such as physics, chemistry, and biology, but its complexity has limited its widespread application. This report introduces a modular and cost-effective droplet microfluidic device for the controlled production of complex emulsions, including oil and aqueous single emulsions, and double emulsions with varying numbers of encapsulated droplets. The droplet sizes can be precisely controlled by easily replacing flat needles and adjusting the needle position within an axially accelerated co-flow field. This modular device not only allows for easy repair and maintenance in case of device clogging or damage but can also be readily expanded to produce complex emulsions. The low-cost and user-friendly nature of the device greatly facilitates the widespread adoption and utilization of droplet microfluidics.
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LncRNAs are vital regulators for lung squamous cell carcinoma (LUSC). However, the detailed role that LINC01133 plays in LUSC is unclear. This work sought to explore the potential function of LINC01133.Levels of LINC01133, miR-30d-5p, and MARCKS were separately tested in both tissues and cells using qRT-PCR. Proliferation was assessed through MTT experiment and apoptosis was detected upon flow cytometry. Transwell experiments were implemented to evaluate migratory and invasive abilities. The interaction between two genes was affirmed through luciferase reporter assay and RNA pull-down experiment. Western blotting measured the protein level of MARCKS. Animal models were established and tissues were taken for IHC analysis of MARCKS and Ki67.LINC01133 was elevated in LUSC and its downregulation could suppress proliferation, migration and invasion but induced apoptosis. LINC01133 interacted with and regulated the binding of miR-30d-5p to MARCKS. LINC01133/miR-30d-5p axis mediated proliferation, apoptosis, migration and invasion in LUSC cells, as well as modulated tumor growth in animal models. LINC01133 interacted with miR-30d-5p to modulate MARCKS expression, contributes to promoted cell proliferation, migration, invasion, and inhibited cell apoptosis in vitro, and promoted tumor growth in vivo. These findings could provide possible therapeutic targets in view of LUSC treatment in the future.
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Aberrant ubiquitin modifications caused by an imbalance in the activities of ubiquitinases and de-ubiquitinases are emerging as important mechanisms underlying non-small cell lung cancer (NSCLC) progression. The deubiquitinating enzyme ubiquitin-specific peptidase 15 (USP15) has been identified as an important factor in oncogenesis and a potential therapeutic target. However, the expression profile and function of USP15 in NSCLC remain elusive. In the present study, we investigated the expression pattern and the potential biological functions of USP15 in NSCLC both in cells and animal models. Our data revealed that USP15 was highly expressed in NSCLC tissues and cells compared with normal counterpart. We subsequently knocked down USP15 expression in two NSCLC cell lines, which significantly suppressed cell proliferation. In addition, knocking down USP15 expression reduced NSCLC cell migration and invasion according to the results from Matrigel-Transwell analysis. NSCLC animal model results showed that USP15 knockdown also reduced NSCLC size. Biochemical analysis revealed that USP15 knockdown inhibited matrix metalloproteinase (MMP)3 and MMP9 expression. Furthermore, high levels of USP15 and MMP3 expression were associated with poor prognosis in NSCLC. In conclusion, the results from the present study suggest that the high expression of USP15 promotes NSCLC tumorigenesis. Therefore, it is proposed that USP15 and MMPs may represent novel biomarkers for NSCLC progression and prognosis.
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Carcinoma de Pulmón de Células no Pequeñas , Neoplasias Pulmonares , Animales , Humanos , Carcinoma de Pulmón de Células no Pequeñas/genética , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/metabolismo , Metaloproteinasa 3 de la Matriz/metabolismo , Movimiento Celular/genética , Línea Celular Tumoral , Proliferación Celular/genética , Pronóstico , Carcinogénesis , Regulación Neoplásica de la Expresión Génica , Proteasas Ubiquitina-Específicas/genética , Proteasas Ubiquitina-Específicas/metabolismoRESUMEN
AIM: It is controversial that whether sleeve lobectomy (SL) should be promoted more worthy than pneumonectomy (PN) in suitable patients. METHODS: We searched all studies that had been published in English from PUBMED and Embase which compared the short-term and long-term outcomes of SL and pneumonectomy (PN) in patients with non-small cell lung cancer (NSCLC). RESULTS: Nineteen studies met our criteria with a combined total of 3878 subjects, of which 1316 (33.9%) underwent SL and 2562 (66.1%) underwent PN. The odds ratio was 0.50 (95% CI: 0.34-0.72) for postoperative mortality, 1.17 (95% CI: 0.82-1.67) for postoperative complications, 0.78 (95% CI: 0.47-1.29) for locoregional recurrences. The risk difference for 1-, 3-, 5- year was 0.11 (95% CI: 0.07-0.14), 0.15 (95% CI: 0.06-0.24), 0.15 (95% CI: 0.09-0.20),respectively. The pooled hazard ratio was 0.63 (95% CI: 0.56-0.71) in favor of SL group. CONCLUSION: SL is more worthy to be done than PN in suitable patients with less mortality and better long-term survival.
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Carcinoma de Pulmón de Células no Pequeñas/cirugía , Neoplasias Pulmonares/cirugía , Neumonectomía/métodos , Carcinoma de Pulmón de Células no Pequeñas/mortalidad , Humanos , Neoplasias Pulmonares/mortalidad , Modelos Estadísticos , Recurrencia Local de Neoplasia , Oportunidad Relativa , Selección de Paciente , Neumonectomía/mortalidad , Complicaciones Posoperatorias/epidemiología , Tasa de Supervivencia , Resultado del TratamientoRESUMEN
This study aimed to investigate the function of long non-coding RNA FOXD2 adjacent opposite strand RNA 1 (lncRNA FOXD2-AS1) during the progression of esophagus cancer (EC) and explore its underlying molecular mechanisms. The level of FOXD2-AS1 in EC tissues and paracancerous tissues was detected by using RT-qPCR; ROC curve was used to evaluate the diagnostic value of FOXD2-AS1 for EC. In addition, CCK8 assay and immunofluorescence staining assay were used to detect the proliferation of Eca-109 and TE-1 cells. To investigate the function of FOXD2-AS1 on cell apoptosis and cell cycle, flow cytometry was performed. To detect the invasion ability of EC cells, transwell invasion assay was performed. Starbase3.0 and Targetscan were used to predict the target genes of FOXD2-AS1 and miR-145-5p, and protein expressions were detected with western blot. We found FOXD2-AS1 was significantly upregulated in EC tissues compared with adjacent normal tissues, which was positively correlated with clinicopathological parameters of patients with EC. Downregulation of FOXD2-AS1 inhibited the proliferation and invasion by inducing apoptosis of EC cells. Moreover, FOXD2-AS1 may regulate the expression of CDK6 by targeting miR-145-3p. Meanwhile, silencing of FOXD2-AS1 caused G1 phase arrest of EC cells by reducing the expression of CDK6. In conclusion, silening FOXD2-AS1 significantly inhibited the proliferation and invasion of EC cells by regulating the miR-145-5p/CDK6 axis. Therefore, FOXD2-AS1 might be used as diagnostic biomarker and therapeutic target for EC.
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Proliferación Celular/genética , Quinasa 6 Dependiente de la Ciclina/genética , Neoplasias Esofágicas/genética , Regulación Neoplásica de la Expresión Génica , MicroARNs/genética , ARN Largo no Codificante/genética , Adulto , Apoptosis/genética , Línea Celular Tumoral , Movimiento Celular/genética , Quinasa 6 Dependiente de la Ciclina/metabolismo , Neoplasias Esofágicas/metabolismo , Neoplasias Esofágicas/patología , Esófago/metabolismo , Esófago/patología , Silenciador del Gen , Humanos , MicroARNs/metabolismo , Persona de Mediana Edad , ARN Largo no Codificante/metabolismo , Transducción de Señal/genéticaRESUMEN
BACKGROUND: Non-small cell lung carcinoma (NSCLC) is a common malignant tumor with poor prognosis. CircRNA-100876 has been considered to be involved in NSCLC. However, the mechanism by which circRNA_100876 mediated the progression of NSCLC remains unclear. METHODS: CCK8 assay and immunofluorescence were used to detect cell proliferation. Flow cytometry and transwell assay were performed to analyze cell apoptosis, migration and invasion, respectively. Verification of possible target for circRNA_100876 and related miR-636 were done using luciferase assay. In addition, western blot was performed to detect the protein expressions in NSCLC cells. RESULTS: Silencing of circRNA_100876 notably inhibited the proliferation of NSCLC cells. Moreover, downregulation of circRNA_100876 significantly induce the apoptosis of NSCLC cells via mediation of apoptosis-related proteins. In addition, silencing of circRNA_100876 significantly inhibited migration and invasion of NSCLC cells. MiR-636 was the downstream target of circRNA_100876. Meanwhile, RET was the direct target of miR-636. Finally, circRNA_100876 shRNA2 notably suppressed the progression of NSCLC through PI3K/Akt signaling. CONCLUSION: CircRNA_100876 knockdown notably suppressed the progression of NSCLC through regulation of miR-636/RET axis, which may serve as a potential target for treatment of NSCLC.
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Carcinoma de Pulmón de Células no Pequeñas/genética , Regulación Neoplásica de la Expresión Génica , Neoplasias Pulmonares/genética , MicroARNs/genética , Interferencia de ARN , ARN Circular/genética , Regiones no Traducidas 3' , Apoptosis/genética , Carcinoma de Pulmón de Células no Pequeñas/metabolismo , Carcinoma de Pulmón de Células no Pequeñas/patología , Línea Celular Tumoral , Movimiento Celular/genética , Proliferación Celular , Regulación hacia Abajo , Silenciador del Gen , Humanos , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/patología , Potencial de la Membrana Mitocondrial/genética , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Transducción de SeñalRESUMEN
BACKGROUND: Esophageal cancer (EC) is one of the aggressive gastrointestinal malignancies. It has been reported that microRNAs (miRNAs) play key roles during the tumorigenesis of EC. To identify novel potential targets for EC, differential expressed miRNAs (DEG) between EC and adjacent normal tissues were analyzed with bioinformatics tool. METHODS: The differential expression of miRNAs between EC and adjacent normal tissues was analyzed. CCK-8 and Ki67 staining were used to detect the cell proliferation. Flow cytometry was performed to test the cell apoptosis. The correlation between miR-7-5p and KLF4 was detected by dual-luciferase report assay. Gene and protein expression in EC cells or in tissues were measured by qRT-PCR and Western blot, respectively. Cell migration and invasion were detected with transwell assay. Xenograft mice model was established to investigate the role of miR-7-5p in EC tumorigenesis in vivo. RESULTS: MiR-7-5p was found to be negatively correlated with the survival rate of patient with EC. In addition, downregulation of miR-7-5p significantly inhibited the growth and invasion of EC cells. Meanwhile, miR-7-5p directly targeted KLF4 in EC cells. Moreover, downregulation of miR-7-5p inhibited the tumorigenesis of EC via inactivating MAPK signaling pathway in vivo. CONCLUSION: Downregulation of miR-7-5p notably suppressed the progression of EC via targeting KLF4. Thus, miR-7-5p might serve as a new target for the treatment of EC.
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Esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EA) are the two most common types of esophageal cancer, which is the sixth highest cause of cancerassociated mortality and the eighth most common cancer worldwide. Gene associated with retinoidinterferon (IFN)induced mortality19 (Grim19) is reported to be a cell death activator that may be used to define mechanisms involved in IFNß and retinoic acidinduced cell death and apoptosis in a number of tumor cell lines. The present study constructed a recombinant adenovirus expressing Grim19 (rAdGrim19) and investigated its therapeutic outcomes in ESCC cells and tumorbearing mice. Grim19 expression was detected in EC109 (ESCC) cells by reverse transcriptionquantitative polymerase chain reaction and western blot analysis. Tumor cell death and apoptosis induced by rAdGrim19 in EC109 cells were analyzed by flow cytometry. The inhibitory effects of rAdGrim19 on EC109 growth were determined by MTT assays. Furthermore, the therapeutic effects of rAdGrim19 were investigated in EC109bearing mice. The results demonstrated that Grim19 mRNA and protein expression was downregulated in EC109 esophageal carcinoma cells compared with Het1A normal esophageal epithelial cells. In addition, EC109 cells exhibited a significant reduction in tumor cell growth in the rAdGrim19 group compared with the control groups. Furthermore, rAdGrim19 increased EC109 cell apoptosis compared with the control group. These results indicated that rAd-Grim-19 may regulate tumor cell growth and apoptosis. Additionally, the results demonstrated that rAdGrim19 led to beneficial outcomes and prolonged the survival of esophageal tumorbearing mice. In conclusion, the present study demonstrated that rAdGrim19 may have potential as an antitumor agent for esophageal neoplasms and may therefore be beneficial for patients with esophageal neoplasms.
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Adenoviridae , Proteínas Reguladoras de la Apoptosis , Apoptosis/genética , Neoplasias Esofágicas , Regulación de la Expresión Génica , NADH NADPH Oxidorreductasas , Transducción Genética , Animales , Proteínas Reguladoras de la Apoptosis/biosíntesis , Proteínas Reguladoras de la Apoptosis/genética , Línea Celular Tumoral , Neoplasias Esofágicas/genética , Neoplasias Esofágicas/metabolismo , Neoplasias Esofágicas/patología , Neoplasias Esofágicas/terapia , Femenino , Humanos , Masculino , Ratones , Ratones Endogámicos BALB C , Ratones Desnudos , Persona de Mediana Edad , NADH NADPH Oxidorreductasas/biosíntesis , NADH NADPH Oxidorreductasas/genética , Ensayos Antitumor por Modelo de XenoinjertoRESUMEN
BACKGROUND: Three-dimensional (3D) simulation of pulmonary vessels and the space between the lesion and adjacent tissues may improve the safety and accuracy of video-assisted thoracoscopic surgery (VATS) for lung. The aim of this study was to evaluate the effect of 3D simulation on the outcome of VATS segmentectomy for ground glass opacity (GGO) in lung. METHODS: We retrospectively analyzed 68 cases of small (≤2 cm) GGO, which were diagnosed as cT1aN0M0 lung cancer, from May 1, 2016 to February 28, 2017 in our institute. All the patients underwent VATS segmentectomy. The patients were divided into "3D" group, 3D preoperative reconstruction simulation in 36 patients and "non-3D" group, 32 patients with only computed tomography (CT). Operation plans were firstly made by CT in all patients, then by 3D simulation only in 3D group. The clinical outcomes, including operation time, blood loss, resection margin distance, length of postoperative stay and postoperative complications were compared between the two groups. RESULTS: There were 21 male and 47 female analyzed, aging from 34 to 72 years (median 57). In 3D group, pathological result showed 8 cases of adenocarcinoma, 23 cases of microinvasive adenocarcinoma (MIA), 5 cases of adenocarcinoma in situ (AIS). In non-3D group, 18 cases of MIA, 9 cases of adenocarcinoma and 5 cases of AIS were diagnosed pathologically. The blood loss, postoperative hospital stay and the incidence of the postoperative complications were similar in both of the groups. There was no 30-day postoperative mortality in either group. The median operation time for the 3D group (111 minute) was shorter than non-3D group (139 minute) (P=0.03). Seven cases (19%) in 3D group changed the original operation plan according to the simulation result with the consideration of adequate resection margin distance. All cases in 3D group had adequate resection margin distance. Four cases (13%) in non-3D group got inadequate resection margin distance, and more lung tissues than the original plan were then resected in these patients (P=0.04). CONCLUSIONS: 3D preoperative simulation may be more precise in operation plan than CT scan and can significantly shorten the operation time in VATS segmentectomy for GGO in lung.
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Growing evidence has demonstrated that the nucleotidebinding oligomerization domainlike receptor family pyrin domain containing 3 (NLRP3) inflammasomemediated inflammatory pathways have been involved in the secondary injury of traumatic brain injury (TBI). In the present study, the authors investigated the effects of hyperbaric oxygen (HBO) therapy on the NLRP3 inflammasome pathway following TBI. Following the evaluation of motor deficits and brain edema, the therapeutic effects of HBO on interleukin (IL)1ß and IL18 expression were assessed, as well as NLRP3 inflammasome activation following TBI. HBO may improve motor score and reduce brain edema, accompanied with the reduction of IL1ß and IL18 during the 7day observation period. Furthermore, HBO suppressed mRNA and protein expression of NLRP3inflammasome components, especially reducing NLRP3 expression in microglia. Thus, these results suggested that HBO alleviates the inflammatory response in experimental TBI via modulating microglial NLRP3inflammasome signaling.
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Lesiones Traumáticas del Encéfalo/terapia , Oxigenoterapia Hiperbárica , Inflamasomas/metabolismo , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismo , Animales , Encéfalo/metabolismo , Encéfalo/patología , Edema Encefálico/metabolismo , Edema Encefálico/terapia , Lesiones Traumáticas del Encéfalo/metabolismo , Lesiones Traumáticas del Encéfalo/patología , Proteínas Adaptadoras de Señalización CARD/metabolismo , Caspasa 1/metabolismo , Interleucina-18/metabolismo , Interleucina-1beta/metabolismo , Masculino , Ratones , Ratones Endogámicos C57BL , Microglía/metabolismo , Microscopía Fluorescente , Actividad Motora , Proteína con Dominio Pirina 3 de la Familia NLR/genética , Transducción de SeñalRESUMEN
Nonsmallcell lung cancer (NSCLC) accounts for ~80% of human lung cancers that result in mortalities worldwide. Metastasisassociated in colon cancer1 (MACC1) has been demonstrated to be significantly expressed in cases of NSCLC and promotes tumor cell migration and metastasis through transactivation of the metastasisinducing hepatocyte growth factor/MET protogene, receptor tyrosine kinase (HGF/MET) signaling pathway. The present study constructed a chimeric antibody (ChantiMACC1) targeting MACC1 and investigated its potential as a molecular therapeutic target in the treatment of NSCLC therapy. The expression of MACC1 was detected by reverse transcriptionquantitative polymerase chain reaction and western blotting in lung cancer cell lines and tissues. MTT assay was used to detect proliferation of A549 cells treated by ChantiMACC1, whereas the functional and regulatory effects of ChantiMACC1 in the migration and metastasis of NSCLC cells was investigated by a cell invasion assay. The therapeutic effect and survival time was observed in animal models. The results demonstrated that MACC1 expression was increased and overexpression of MACC1 promoted the progression of the cell cycle, significantly promoted NSCLC cell growth and enhanced tumor migration and invasion through the HGF/MET signaling pathway. It was further demonstrated that ChantiMACC1 efficiently suppressed MACC1 expression and significantly inhibited NSCLC cell proliferation, migration and invasion by blocking the HGF/MET signaling pathway. The data revealed that ChantiMACC1 was not only beneficial for tumor remission, however additionally contributed to the longterm survival of NSCLC bearing mice. The findings of the present study indicated that MACC1 was significantly upregulated and promoted tumor cell growth and migration in NSCLC cells and tissues via transactivation of the metastasisinducing HGF/MET signaling pathway. However, ChantiMACC1significantly inhibited tumor growth and metastasis, which suggested that MACC1 may be essential for tumor initiation and progression by negatively regulating tumor suppressors.
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Anticuerpos Monoclonales/farmacología , Carcinoma de Pulmón de Células no Pequeñas/patología , Proliferación Celular/efectos de los fármacos , Neoplasias Pulmonares/patología , Factores de Transcripción/inmunología , Células A549 , Animales , Anticuerpos Monoclonales/genética , Anticuerpos Monoclonales/metabolismo , Anticuerpos Monoclonales/uso terapéutico , Carcinoma de Pulmón de Células no Pequeñas/tratamiento farmacológico , Carcinoma de Pulmón de Células no Pequeñas/metabolismo , Línea Celular Tumoral , Movimiento Celular/efectos de los fármacos , Regulación hacia Abajo/efectos de los fármacos , Transición Epitelial-Mesenquimal/efectos de los fármacos , Femenino , Factor de Crecimiento de Hepatocito/metabolismo , Humanos , Neoplasias Pulmonares/tratamiento farmacológico , Neoplasias Pulmonares/metabolismo , Ratones , Ratones Endogámicos C57BL , Microscopía Fluorescente , Proteínas Proto-Oncogénicas c-met/metabolismo , Proteínas Recombinantes de Fusión/biosíntesis , Proteínas Recombinantes de Fusión/genética , Proteínas Recombinantes de Fusión/farmacología , Proteínas Recombinantes de Fusión/uso terapéutico , Transducción de Señal/efectos de los fármacos , Transactivadores , Factores de Transcripción/genética , Factores de Transcripción/metabolismo , Trasplante HeterólogoRESUMEN
Biomarkers that can serve as diagnostic and prognostic indicators of esophageal squamous cell carcinoma (ESCC) are urgently needed to help improve patient outcomes. Here, the expression of epidermal growth factor receptor (EGFR) and costimulatory molecule B7-H3, both of which have been implicated in tumor onset and progression in certain tumors, was investigated in relation to the clinical characteristics and survival outcomes of patients with ESCC. ESCC tissue samples were analyzed for 100 patients. Tumor and patient characteristics were recorded. Tissues were investigated for EGFR and B7-H3 staining by immunohistochemistry. Patients were followed for up to 96 months to determine overall survival (OS) and progression-free survival (PFS). High expression for EGFR (68.0%) and B7-H3 (66.0%) was observed in the majority of cases. High expression of either EGFR or B7-H3 was correlated with tumor invasion depth and clinical stage (P<0.05). Further, high expression of either EGFR or B7-H3 was correlated with worse survival outcomes. The estimated OS (38.1 months) and PFS (13.4 months) of patients with high expression of EGFR were lower than those of patients with low expression (69.3 and 68.1 months, P<0.05). The estimated OS (31.1 months) and PFS (13.1 months) of patients with high expression of B7-H3 were also lower than those of patients with low expression (69.3 and 66.6 months, P<0.05). Indeed, Cox multiple regression showed that OS and PFS were correlated with EGFR (relative risk =1.853, 1.875, respectively) and B7-H3 (relative risk =1.886, 2.061, respectively) (all P<0.05) expression level. Thus, EGFR and B7-H3 are highly expressed in tumor tissues of patients with ESCC. Their expression levels are correlated with tumor severity and survival, and therefore these may be viable biomarkers to aid in prognosis determination.
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BACKGROUND: We aimed to evaluate the value of (18)FDG PET-CT for detection of regional nodal metastasis in patients with esophageal cancer before surgery. METHODS: A computer search about PET-CT original articles was conducted from January 2000 to December 2012. The reference standard was histopathologic analysis. Two reviewers independently searched articles and extracted data. Sensitivity, specificity, diagnostic odds ratio, and likelihood ratio were pooled for PET-CT using bivariate models. Summary receiver operating characteristic (SROC) curves were also used to summarize overall test performance. RESULTS: Across all seven studies on a per-station analysis (2232 stations), the pooled sensitivity and speciï¬city with 95% confidence interval for PET-CT were 0.62 (0.40-0.79) and 0.96 (0.93-0.98). Across all 6 studies on a per-patient analysis (245 patients), corresponding values for PET-CT were 0.55 (0.34-0.74) and 0.76 (0.66-0.83). CONCLUSIONS: (18)FDG PET-CT had lower sensitivity and accuracy for detection of regional nodal metastasis in patients with esophageal cancer before surgery.