miR-101 sensitizes A549 NSCLC cell line to CDDP by activating caspase 3-dependent apoptosis

Yin, Ji-Qing; Wang, Mingguo; Jin, Cuixiang; Qi, Qing-guo

doi:10.3892/ol.2013.1725

Cited by 26 publications

(21 citation statements)

References 26 publications

(28 reference statements)

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“…Wang et al [131] reported that up-regulation of miR-138 gave rise to increased cell apoptosis and chemosensitivity of cisplatin-resistant A549 cells through down-regulation of the excision repair cross-complementation group 1 (ERCC1). In a recent study, Yin et al [133] demonstrated that over-expression of miR-101 sensitized A549 cells to cisplatin via the activation of caspase-3-dependent apoptosis. In a recent study, Yin et al [133] demonstrated that over-expression of miR-101 sensitized A549 cells to cisplatin via the activation of caspase-3-dependent apoptosis.…”

Section: Chemotherapymentioning

confidence: 99%

Non-small-cell lung cancer and miRNAs: novel biomarkers and promising tools for treatment

et al. 2015

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Lung cancer is the leading cause of cancer-related death worldwide, with approximately 80-85% of cases being non-small-cell lung cancer (NSCLC). The miRNAs are small non-coding RNAs that regulate gene expression at a post-transcriptional level by either degradation or inhibition of the translation of target genes. Evidence is mounting that miRNAs exert pivotal effects in the development and progression of human malignancies, including NSCLC. A better understanding of the role that miRNAs play in the disease will contribute to the development of new diagnostic biomarkers and individualized therapeutic tools. In the present review, we briefly describe the role of miRNAs in NSCLC as well as the possible future of these discoveries in clinical applications.

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Section: Chemotherapymentioning

confidence: 99%

Non-small-cell lung cancer and miRNAs: novel biomarkers and promising tools for treatment

et al. 2015

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“…miR-101 is a miRNA that regulates a variety of tumor-related biological processes by modulating the expression of several target genes at the transcript or protein level (25,26). Normally, miR-101 inhibits the expression of lung cancer promoting genes (17,27). In this study, we observed a miR-101 binding site at 3891–3912 nt of the DNMT3A 3′-UTR.…”

Section: Discussionmentioning

confidence: 99%

“…Loss and gain of miRNA functions contribute to the development of cancer through the upregulation of oncogenes and silencing of TSGs. miR-101 acts as a tumor suppressor, which regulates growth, apoptosis, migration and invasion of various tumor cells (15–17). However, miR-101 has not been clearly identified as a selective regulator of DNMT3A in NSCLC.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-101 suppresses progression of lung cancer through the PTEN/AKT signaling pathway by targeting DNA methyltransferase 3A

et al. 2016

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It is well established that transcriptional silencing of critical tumor suppressor genes by DNA methylation is a fundamental process in the initiation of lung cancer. However, the involvement of microRNAs (miRNAs) in restoring abnormal DNA methylation patterns in lung cancer is not well understood. Therefore, and since miRNA-101 is complementary to the 3′-untranslated region of DNA methyltransferase 3A (DNMT3A), we investigated whether miRNA-101 could restore normal DNA methylation patterns in lung cancer cell lines. Bioinformatics has indicated that DNMT3A is a major target of miR-101. In addition, the overexpression of miR-101 downregulates DNMT3A. Using a methylation-specific polymerase chain reaction assay, we demonstrated that methylation of the phosphatase and tensin homolog (PTEN) promoter was reduced in A549 cells transfected with miR-101, but not in the transfected control. Furthermore, overexpression of miR-101 and silencing of DNMT3A suppressed lung cell proliferation and S/G2 transition, and increased apoptosis through the PTEN/AKT pathway in vitro. Furthermore, we observed the opposite phenomenon in A549 cells transfected with a miR-101 inhibitor. Subsequent investigation revealed that overexpression of miR-101 significantly inhibited the tumorigenicity of A549 cells in a nude mouse xenograft model. These results demonstrate that miR-101 affects lung cancer progression through the PTEN/AKT signaling pathway by targeting DNMT3A in lung cells, suggesting that miR-101 may be a novel potential therapeutic strategy in lung cancer treatment.

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“…miR-101 has been demonstrated to participate in the regulation of various cancers (11,12). For example, miR-101 was demonstrated to be a potent inhibitor of autophagy in breast cancer cells and the inhibition of miR-101 sensitized breast cancer cells to drug-mediated cell death (10).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of microRNA-101 attenuates hypoxia/reoxygenation-induced apoptosis through induction of autophagy in H9c2 cardiomyocytes

Jiang

Chen

et al. 2015

Molecular Medicine Reports

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Abstract. Autophagy is a cellular self-catabolic process responsible for the degradation of proteins and organelles. Autophagy is able to promote cell survival in response to stress, and increased autophagy amongst cardiomyocytes has been identified in conditions of heart failure, starvation and ischemia/reperfusion. However, the detailed regulatory mechanisms underlying autophagy in heart disease have remained elusive. MicroRNAs (miRNAs) have been implicated in the regulation of autophagy in cells under stress. In the present study, the protective effect of miRNA (miR)-101 on hypoxia/reoxygenation (H/R)-induced cardiomyocyte apoptosis was investigated. It was revealed that H/R induced apoptosis in H9c2 cardiomyocytes, accompanied by a downregulation of miR-101 expression. Further investigation identified Ras-related protein Rab-5A (RAB5A) as a direct target of miR-101. RAB5A was previously reported to be involved in autophagy; therefore, the present study further focused on the role of miR-101 in the regulation of autophagy under H/R and found that the inhibition of miR-101 attenuated H/R-induced apoptosis, at least partially, via the induction of autophagy. In conclusion, the results of the present study revealed a beneficial effect of miR-101 inhibition on H/R-induced apoptosis in cardiomyocytes, indicating that miR-101 inhibition may present a potential therapeutic agent in the treatment or prevention of heart diseases. IntroductionAutophagy is a cellular self-catabolic process responsible for the degradation of long-lived proteins and organelles. During autophagy, cytoplasmic constituents are sequestered into autophagosomes and degraded via the lysosomal pathway (1).Autophagy is able to promote cell survival in response to stress. However, progressive autophagy also induces cell death (2). Therefore, autophagy not only has a crucial role in the regulation of normal development, but dysregulated or defective autophagy is associated with disease.MicroRNAs (miRNAs) are a group of endogenous, non-coding, single-strand, small RNAs of 22-25 nucleotides, which regulate gene expression at the post-transcriptional level, predominantly through base pairing with the 3'-untranslated region (3'-UTR) of target mRNAs, which results in mRNA degradation or translational repression (3). It has been revealed that miRNAs regulate >30% of genes, which are associated with almost all major cellular processes, including cell proliferation, differentiation, apoptosis and migration, as well as immune responses (4). Myocardial tissue injury induced by ischemia and hypoxia is a major factor underlying the development of fatal diseases. The main cause of myocardial ischemic injury is myocardial cell apoptosis induced by myocardial hypoxia (5). Furthermore, subsequent reoxygenation may further aggravate the damage (6). Multiple miRNAs have been shown to function as protectors against hypoxia/reoxygenation (H/R)-induced myocardial injury (7-9). However, the specific molecular mechanisms underlying this effect have remained elusive.Accumu...

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miR-101 sensitizes A549 NSCLC cell line to CDDP by activating caspase 3-dependent apoptosis

Cited by 26 publications

References 26 publications

Non-small-cell lung cancer and miRNAs: novel biomarkers and promising tools for treatment

Non-small-cell lung cancer and miRNAs: novel biomarkers and promising tools for treatment

MicroRNA-101 suppresses progression of lung cancer through the PTEN/AKT signaling pathway by targeting DNA methyltransferase 3A

Inhibition of microRNA-101 attenuates hypoxia/reoxygenation-induced apoptosis through induction of autophagy in H9c2 cardiomyocytes

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