miR-137 inhibits the proliferation of human non-small cell lung cancer cells by targeting SRC3

Chen, Ruilin; Zhang, Yongqing; Zhang, Chengcheng; Wu, Hua; Yang, Sheng

doi:10.3892/ol.2017.5904

Cited by 28 publications

(23 citation statements)

References 35 publications

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“…For instance, coiled-coil domain containing 106 promoted proliferation of A549 and H1299 cells by upregulating CCNA2 expression (45). In another report, miR-137 and miR-30a inhibited tumor growth by inducing cell-cycle arrest and downregulating cell cycle-associated regulators, including CCNA2 (46,47). In addition, the gene E2F1 is an important transcription factor and is one of the most important pro-metastatic genes.…”

Section: Discussionmentioning

confidence: 98%

Regulatory interactions between long noncoding RNA LINC00968 and miR‑9‑3p in non‑small cell lung cancer: A bioinformatic analysis based on miRNA microarray, GEO and TCGA

Chen

Shang

et al. 2018

Oncol Lett

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Long non-coding RNAs (lncRNAs) have been demonstrated to mediate carcinogenesis in various types of cancer. However, the regulatory role of lncRNA LINC00968 in lung adenocarcinoma remains unclear. The microRNA (miRNA) expression in LINC00968-overexpressing human lung adenocarcinoma A549 cells was detected using miRNA microarray analysis. miR-9-3p was selected for further analysis, and its expression was verified in the Gene Expression Omnibus (GEO) database. In addition, the regulatory axis of LINC00968 was validated using The Cancer Genome Atlas (TCGA) database. Results of the GEO database indicated miR-9-3p expression in lung adenocarcinoma was significantly higher compared with normal tissues. Functional enrichment analyses of the target genes of miR-9-3p indicated protein binding and the AMP-activated protein kinase pathway were the most enriched Gene Ontology and KEGG terms, respectively. Combining target genes with the correlated genes of LINC00968 and miR-9-3p, 120 objective genes were obtained, which were used to construct a protein-protein interaction (PPI) network. Cyclin A2 (CCNA2) was identified to have a vital role in the PPI network. Significant correlations were detected between LINC00968, miR-9-3p and CCNA2 in lung adenocarcinoma. The LINC00968/miR-9-3p/CCNA2 regulatory axis provides a new foundation for further evaluating the regulatory mechanisms of LINC00968 in lung adenocarcinoma.

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Section: Discussionmentioning

confidence: 98%

Regulatory interactions between long noncoding RNA LINC00968 and miR‑9‑3p in non‑small cell lung cancer: A bioinformatic analysis based on miRNA microarray, GEO and TCGA

Chen

Shang

et al. 2018

Oncol Lett

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“…miR-137 is an important tumor suppressor. It regulates cancer cell proliferation, migration, apoptosis, and autophagy in many types of cancers by targeting XIAP, FUNDC1, NIX, SRC3, and more [ 38 – 40 ]. In the present study, we introduced miR-137 as the first miRNA that regulates erastin- and RSL3-induced ferroptosis in melanoma (Fig.…”

Section: Discussionmentioning

confidence: 99%

miR-137 regulates ferroptosis by targeting glutamine transporter SLC1A5 in melanoma

et al. 2018

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Ferroptosis is a regulated form of cell death driven by small molecules or conditions that induce lipid-based reactive oxygen species (ROS) accumulation. This form of iron-dependent cell death is morphologically and genetically distinct from apoptosis, necroptosis, and autophagy. miRNAs are known to play crucial roles in diverse fundamental biological processes. However, to date no study has reported miRNA-mediated regulation of ferroptosis. Here we show that miR-137 negatively regulates ferroptosis by directly targeting glutamine transporter SLC1A5 in melanoma cells. Ectopic expression of miR-137 suppressed SLC1A5, resulting in decreased glutamine uptake and malondialdehyde (MDA) accumulation. Meanwhile, antagomir-mediated inactivation of endogenous miR-137 increased the sensitivity of melanoma cells to erastin- and RSL3-induced ferroptosis. Importantly, knockdown of miR-137 increased the antitumor activity of erastin by enhancing ferroptosis both in vitro and in vivo. Collectively, these data indicate that miR-137 plays a novel and indispensable role in ferroptosis by inhibiting glutaminolysis and suggest a potential therapeutic approach for melanoma.

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“…miR-98 inhibits cell proliferation via targeting Col1A1 in human hypertrophic scar fibroblasts [16], and miR-181b may be a potential therapy for hypertrophic scar [17]. Furthermore, miR-137 was decreased in several cancers, and a low miR-137 level was an independent risk factor for cancer [18][19][20][21][22]. MiR-137 could promote the recovery of spinal cord injury [23,24].…”

Section: Discussionmentioning

confidence: 99%

miR-137 Inhibits Proliferation and Metastasis of Hypertrophic Scar Fibroblasts via Targeting Pleiotrophin

Zhang

Guo

Qiang

et al. 2018

Cell Physiol Biochem

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Background/Aims: There are few effective treatment options for hypertrophic scars. MircoRNAs are a class of small, noncoding RNAs involved in multiple biological functions. Methods: Gene chip screening was used to screen out the differential expression of miRNAs in hypertrophic scars and normal tissues. Western blot and real-time PCR were used to confirm the expression of pleiotrophin (PTN) in hypertrophic scars. After analyze the correlation between PTN and miR-137 using correlation analysis, we used miRDB software to analyze the binding sites of miR-137 and PTN. Luciferase reporter gene, western blot and real-time PCR experiments were used to detect the regulatory effect of miR-137 on PTN. MTT and transwell assay were used to detect the effect of miR-137 on proliferation and metastasis. Western blot and real-time PCR were used to detect the regulatory effects of miR-137 on cyclin B1, matrix metalloproteinase 9 (MMP9), α-smooth muscle actin (α-SMA), vimentin, and type-I collagen (COL1A). Finally, miR-137 inhibitor was transfected into fibroblasts which was silent PTN, and the proliferation and migration of cells were detected by MTT and transwell. Western blot and real-time PCR were used to detect the expression of related proteins. Results: Various miRNAs was abnormal expressed in hypertrophic scars. miR-137 was decreased in hypertrophic scar, however PTN was up regulated in hypertrophic scars. miR-137 induced proliferation and metastasis in fibroblasts. This effect was accompanied by decreased expression of cyclin B1, MMP9, α-SMA, vimentin, and COL1A mediated via the target of PTN. Conclusion: Modulation of miR-137 expression in fibroblasts could provide an important therapeutic strategy for hypertrophic scars.

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miR-137 inhibits the proliferation of human non-small cell lung cancer cells by targeting SRC3

Cited by 28 publications

References 35 publications

Regulatory interactions between long noncoding RNA LINC00968 and miR‑9‑3p in non‑small cell lung cancer: A bioinformatic analysis based on miRNA microarray, GEO and TCGA

Regulatory interactions between long noncoding RNA LINC00968 and miR‑9‑3p in non‑small cell lung cancer: A bioinformatic analysis based on miRNA microarray, GEO and TCGA

miR-137 regulates ferroptosis by targeting glutamine transporter SLC1A5 in melanoma

miR-137 Inhibits Proliferation and Metastasis of Hypertrophic Scar Fibroblasts via Targeting Pleiotrophin

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