RESUMO
OBJECTIVE: The study investigated the association between FLG-AS1 and cervical cancer prognosis and the interaction mechanism between FLG-AS1 and miR-147b in order to identify potential therapeutic targets for cervical cancer. METHODS: In this study, tissue samples and clinicopathological characteristics were obtained from 125 cervical cancer patients. FLG-AS1 expression levels in the samples were detected by polymerase chain reaction assay. CCK-8 and Transwell assays were used to evaluate FLG-AS1's impact on cervical cancer cell proliferation and metastasis. The mechanism of action of FLG-AS1 and miR-147b was probed by a dual luciferase reporter gene assay. The prognostic nature of FLG-AS1 in cervical cancer was explored by a series of statistical approaches. RESULTS: In cervical cancer cells and tissues, FLG-AS1 expression is markedly downregulated. FLG-AS1 inhibits the activities of cervical cancer cells by negatively regulating miR-147b expression. Patients with cervical cancer have a poor prognosis when FLG-AS1 expression is low. CONCLUSION: FLG-AS1 may be considered as a novel cervical cancer prognostic biomarker candidate, which affects cancer cell progression by negatively regulating miR-147b.
Assuntos
Proliferação de Células , Progressão da Doença , Proteínas Filagrinas , Regulação Neoplásica da Expressão Gênica , MicroRNAs , RNA Longo não Codificante , Neoplasias do Colo do Útero , Feminino , Humanos , Pessoa de Meia-Idade , Biomarcadores Tumorais/genética , Biomarcadores Tumorais/metabolismo , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , MicroRNAs/genética , MicroRNAs/metabolismo , Prognóstico , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Neoplasias do Colo do Útero/genética , Neoplasias do Colo do Útero/patologiaRESUMO
Purpose: This study aimed to detect the role and mechanism of circTMEM59 in pancreatic ductal adenocarcinoma (PDAC). Methods: 66 paired PDAC tissues and normal samples were harvested from patients diagnosed and undergoing pancreatic cancer surgery in our hospital. The expression of circTMEM59 in PDAC tissues and cell lines was detected. Based on bioinformatics information, the circTMEM59 mimics, miR-147b mimics, miR-147b inhibitor and si-suppressor of cytokine signaling 1 (SOCS1) were transfected into PDAC cells. The expression levels of circTMEM59, miR-147b and SOCS1 were detected by quantitative real-time polymerase chain reaction (qRT-PCR). RNA interaction was confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Cell invasion and proliferation were evaluated by Transwell and Cell Counting Kit-8 (CCK-8) assays. The protein expression was detected by Western blot. Results: CircTMEM59 was confirmed to be downregulated in PDAC tumor tissues and cells. Low expression of circTMEM59 was closely correlated with the short survival time and poor clinicopathological characteristics. By up-regulating the expression of circTMEM59 in PDAC cells, cell proliferation, invasion and epithelial-mesenchymal transition (EMT) were inhibited. More importantly, miR-147b could be sponged by circTMEM59, and knockdown of miR-147b inhibited progression of PDAC cells. Further study revealed that SOCS1 was targeted by miR-147b. SOCS1 expression was negatively related to miR-147b expression and positively related to circTMEM59 expression in PDAC tissues. Upregulated miR-147b and downregulated SOCS1 could rescue the effects of circTMEM59 on cell proliferation, EMT and invasion. Conclusion: Our data indicated that circTMEM59 inhibited cell proliferation, invasion and EMT of PDAC by regulating miR-147b/SOCS1 axis.