Background： MicroRNAs （miRNAs） have been extensively studied over the decades and have been identified as potential molecular targets for cancer therapy. To date, many miRNAs have been found participating in the tu...Background： MicroRNAs （miRNAs） have been extensively studied over the decades and have been identified as potential molecular targets for cancer therapy. To date, many miRNAs have been found participating in the tumorigenesis of non-small cell lung cancer （NSCLC）. The present study was designed to evaluate the functions of miR-125b-1-3p in NSCLC cells. Methods： MiR-125b-1-3p expression was detected in tissue samples from 21 NSCLC patients and in NSCLC cell lines using the real-time polymerase chain reaction. A549 cell lines were transfected with a miR-125b-1-3p mimic or miR-125b-1-3p antisense. Cell counting kit-8, wound healing, Matrigel invasion assays, and flow cytometry were used to assess the effects of these transfections on cell growth, migration, invasion, and apoptosis, respectively. Western blotting was used to detect apoptosis-related proteins, expression ofS 1PR 1, and the phosphorylation status of STAT3. Significant differences between groups were estimated using Student＇s t-test or a one-way analysis of variance. Results： MiR-125b-1-3p was downregulated in NSCLC samples and cell lines. Overexpression ofmiR-125b-1-3p inhibited NSCLC cell proliferation （37.8 ± 9.1%, t = 3.191, P = 0.013）, migration （42.3 ± 6.7%, t = 6.321, P = 0.003）, and invasion （57.6 ±1 1.3%, t =4.112, P = 0.001） and simultaneously induced more NSCLC cell apoptosis （2.76 ± 0.78 folds, t = 3.772, P = 0.001）. MiR-125b-l-3p antisense resulted in completely opposite results. SIPRI was found as the target gene ofmiR-125b-1-3p. Overexpression of miR-125b-1-3p inhibited S I PRI protein expression （27.4 ± 6.1% of control, t = 4.083, P = 0.007）. In addition, SIPR1 siRNA decreased STAY3 phosphorylation （16.4 ±0.14% of control, t = 3.023, P = 0.015）, as in cells overexpressing miR-125b-1-3p （16.7 ± 0.17% of control, t = 4.162, P = 0.026）. Conclusion： Our results suggest that miR-125b-1-3p exerts antitumor functions in NSCLC cells by targeting SIPR1.展开更多
文摘Background： MicroRNAs （miRNAs） have been extensively studied over the decades and have been identified as potential molecular targets for cancer therapy. To date, many miRNAs have been found participating in the tumorigenesis of non-small cell lung cancer （NSCLC）. The present study was designed to evaluate the functions of miR-125b-1-3p in NSCLC cells. Methods： MiR-125b-1-3p expression was detected in tissue samples from 21 NSCLC patients and in NSCLC cell lines using the real-time polymerase chain reaction. A549 cell lines were transfected with a miR-125b-1-3p mimic or miR-125b-1-3p antisense. Cell counting kit-8, wound healing, Matrigel invasion assays, and flow cytometry were used to assess the effects of these transfections on cell growth, migration, invasion, and apoptosis, respectively. Western blotting was used to detect apoptosis-related proteins, expression ofS 1PR 1, and the phosphorylation status of STAT3. Significant differences between groups were estimated using Student＇s t-test or a one-way analysis of variance. Results： MiR-125b-1-3p was downregulated in NSCLC samples and cell lines. Overexpression ofmiR-125b-1-3p inhibited NSCLC cell proliferation （37.8 ± 9.1%, t = 3.191, P = 0.013）, migration （42.3 ± 6.7%, t = 6.321, P = 0.003）, and invasion （57.6 ±1 1.3%, t =4.112, P = 0.001） and simultaneously induced more NSCLC cell apoptosis （2.76 ± 0.78 folds, t = 3.772, P = 0.001）. MiR-125b-l-3p antisense resulted in completely opposite results. SIPRI was found as the target gene ofmiR-125b-1-3p. Overexpression of miR-125b-1-3p inhibited S I PRI protein expression （27.4 ± 6.1% of control, t = 4.083, P = 0.007）. In addition, SIPR1 siRNA decreased STAY3 phosphorylation （16.4 ±0.14% of control, t = 3.023, P = 0.015）, as in cells overexpressing miR-125b-1-3p （16.7 ± 0.17% of control, t = 4.162, P = 0.026）. Conclusion： Our results suggest that miR-125b-1-3p exerts antitumor functions in NSCLC cells by targeting SIPR1.
