Background/Aims: A growing body of evidence indicates that the abnormal expression of microRNAs (miRNAs) play an important role in sensitizing the cellular response to ionizing radiation (IR). The aim of this study was to investigate whether the expression of miR-124 correlated with radiosensitivity in the context of non-small-cell lung carcinoma (NSCLC). Methods: Quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to quantify miR-124 expression in NSCLC tissues and cell lines. The role of miR-124 in NSCLC proliferation and radiosensitivity was analyzed using CCK-8 and flow cytometry apoptosis assays. Luciferase activity assays, RT-PCR, and Western blot assays were performed to confirm the target gene of miR-124. Results: In this study, we found that miR-124 was downregulated both in clinical NSCLC samples and in cell lines. miR-124 inhibited the proliferation of NSCLC cells and enhanced the apoptosis of NSCLC cells exposed to ionizing radiation. We identified signal transducer and activator of transcription 3 (STAT3) as a direct target of miR-124 by using target prediction algorithms and luciferase assays. Overexpression of STAT3 in A549 cell lines restored the enhanced radiosensitivity induced by miR-124. Conclusion: Taking these observations into consideration, we illustrated that miR-124 is a potential target for enhancing the radiosensitivity of NSCLC cells by targeting STAT3.
Background The POU domain class 5 transcription factor 1B (POU5F1B), is a pseudogene that is homologous to octamer-binding transcription factor 4 (OCT4), and is located adjacent to the MYC gene on human chromosome 8q24. POU5F1B has been reported to be transcribed in several types of cancer, but its role in cervical cancer remains unclear. This study aimed to investigate the expression and function of POU5F1B in tissue samples of human cervical cancer and in cervical cancer cell lines in vitro . Material/Methods Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to quantify POU5F1B expression in cervical cancer tissues and in SiHa, HeLa, CaSki, and C33A human cervical cancer cell lines. Functional in vitro studies included analysis of the effects of POU5F1B expression on cervical cancer cell proliferation, migration, and apoptosis using a Cell Counting Kit-8 (CCK-8) assay, cell migration assays, and flow cytometry. Luciferase activity assays, qRT-PCR, and Western blot were performed to confirm the expression of POU5F1B. Results POU5F1B was significantly upregulated in cervical cancer tissues and cell lines. Interference with the expression of POU5F1B significantly inhibited cell proliferation, apoptosis, migration and invasion, and induced apoptosis in vitro . Western blot demonstrated that POU5F1B could modulate the expression of the OCT4 protein. Conclusions POU5F1B was upregulated in cervical cancer and down-regulation inhibited cell proliferation and migration and induced apoptosis in cervical cancer cell lines by modulating OCT4. Further studies are required to determine whether POU5F1B might be a diagnostic or prognostic biomarker or therapeutic target in cervical cancer.
Background POU5F1B, serving as a carcinogen, participates in radiosensitivity of several tumors. However, in esophageal cancer, its potential mechanism and function in regulating radiosensitivity remain unclear. Material/Methods The expression level of POU5F1B was detected in plasma of esophageal tumor patients and cancer cell lines. The effect of POU5F1B knockdown on cell proliferation and colony formation was determined using CCK-8 assay and colony formation assay. Cell apoptosis rate was detected by flow cytometry. Results POU5F1B expression level declined after radiotherapy in the plasma of esophageal cancer patients (p=0.025). Compared with HEEPIC, the level of POU5F1B was upregulated in ECA109 (p<0.01), ECA9706 (p<0.01), KYSE410 (p<0.01), and KYSE510 (p=0.036). The silencing of POU5F1B played a role in inhibiting colony formation. After radiotherapy, the apoptosis rates in the ECA109 with 4Gy si-POU5F1B group and 4Gy si-NC group were 39.1±0.1% and 35.3±0.1%, respectively (p=0.0193). The rate was 21.00±0.1 and 29.1±0.1% (p<0.0072) in the si-NC group and si-POU5F1B group, respectively. For proliferation rate, 4Gy si-POU5F1B ECA109 performed better than 4Gy si-NC. Conclusions Radiotherapy contributed to the decline in the expression level of POU5F1B in plasma, which was upregulated in ECA109, ECA9706, KYSE410, and KYSE510, but not in HEEPIC. The knockdown of POU5F1B increased the radiosensitivity of esophageal cancer cell lines.
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