MicroRNA-138 suppresses invasion and promotes apoptosis in head and neck squamous cell carcinoma cell lines

Liu, Xiqiang; Jiang, Lu; Wang, Anxun; Yu, Jinsheng; Shi, Fei; Zhou, Xiaofeng

doi:10.1016/j.canlet.2009.05.030

Cited by 190 publications

(198 citation statements)

References 49 publications

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“…In nasopharyngeal carcinoma, miR-138 markedly decreased cell proliferation and colony formation in vitro, and tumorigenesis in vivo (37). In head and neck squamous cell carcinoma, ectopic transfection with miR-138 inhibited cell invasion, and enhanced cell-cycle arrest and apoptosis (22). The evidence from these prior studies, together with the findings of the present study, indicates that miR-138 acts as a tumor suppressor in cancer.…”

Section: Discussionsupporting

confidence: 76%

“…miR-138/SP1-based targeted therapy could therefore represent a promising therapeutic strategy for HCC patients. Downregulation of miR-138 has been reported in diverse types of human cancer, including anaplastic thyroid carcinoma (21), head and neck squamous cell carcinoma (22), clear cell renal cell carcinoma (23), ovarian cancer (24), glioblastoma (25), colorectal cancer (26), non-small cell lung cancer (NSCLC) (27), pancreatic cancer (28) and breast cancer (29). Furthermore, reduced miR-138 expression was associated with a number of cancer characteristics.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA‑138 targets SP1 to inhibit the proliferation, migration and invasion of hepatocellular carcinoma cells

et al. 2017

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Abstract. The identification of microRNAs (miRNAs/miRs) has enabled the improved understanding of the carcinogenesis and progression of hepatocellular carcinoma (HCC). miRNAs are small non-coding RNAs comprised of 19-24 nucleotides that regulate the expression of target genes. In the present study, miR-138 was demonstrated to be downregulated in human HCC tissues and cell lines. Restoration of miR-138 expression repressed the proliferation, migration and invasion of HCC cells. Furthermore, specificity protein 1 (SP1) was identified as a target gene of miR-138 in HCC using bioinformatics analysis, luciferase reporter assay, reverse transcription-quantitative polymerase chain reaction and western blot analysis. Knockdown of SP1 produced similar suppressive effects to those induced by miR-138 overexpression in HCC cells. These results indicate that miR-138 targeted SP1 to repress the growth, migration and invasion of HCC cells, and may therefore represent a therapeutic target in human HCC.

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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

MicroRNA‑138 targets SP1 to inhibit the proliferation, migration and invasion of hepatocellular carcinoma cells

et al. 2017

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“…miR-138 was reported to act as a tumor suppresser and serve as a therapeutic target in head and neck squamous cell carcinoma patients (43) and be involved in regulation of ABCB1 transcription (27). Therapy targeting miR-138 may be a therapeutic approach to inhibit ABCB1 in NSCLC cells.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of ABCB1 Overcomes Cancer Stem Cell–like Properties and Acquired Resistance to MET Inhibitors in Non–Small Cell Lung Cancer

Sugano

Seike

Noro

et al. 2015

Molecular Cancer Therapeutics

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Patients with non-small cell lung cancer (NSCLC) EGFR mutations have shown a dramatic response to EGFR inhibitors (EGFR-TKI). EGFR T790M mutation and MET amplification have been recognized as major mechanisms of acquired resistance to EGFR-TKI. Therefore, MET inhibitors have recently been used in NSCLC patients in clinical trials. In this study, we tried to identify the mechanism of acquired resistance to MET inhibitors. We analyzed the antitumor effects of two MET inhibitors, PHA-665752 and crizotinib, in 10 NSCLC cell lines. EBC-1 cells with MET amplification were the only cells that were sensitive to both MET inhibitors. We established PHA-665752-resistant EBC-1 cells, namely EBC-1R cells. Activation of KRAS, EGFR, and FGFR2 signaling was observed in EBC-1R cells by FISH and receptor tyrosine kinase phosphorylation antibody arrays. EBC-1R cells also showed overexpression of ATP-binding cassette subfamily B member 1 (ABCB1) as well as phosphorylation of MET. EBC-1R cells grew as cell spheres that exhibited cancer stem cell-like (CSC) properties and epithelial-mesenchymal transition (EMT). The level of miR-138 that targeted ABCB1 was decreased in EBC-1R cells. ABCB1 siRNA and the ABCB1 inhibitor elacridar could reduce sphere numbers and suppress EMT. Elacridar could also reverse resistance to PHA-665752 in EBC-1R cells. Our study demonstrated that ABCB1 overexpression, which was associated with CSC properties and EMT, was involved in the acquired resistance to MET inhibitors. Inhibition of ABCB1 might be a novel therapeutic strategy for NSCLC patients with acquired resistance to MET inhibitors.

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“…Downregulation of miR-7 in breast cancer has also been proven in the study by Kong et al (42), who demonstrated the inhibition of epithelial-to-mesenchymal transition and metastasis of breast cancer cells via targeting FAK expression. Previously studies have demonstrated that miR-7 is also downregulated in advanced tongue squamous cell carcinoma cell lines (43,44). Therefore, our current results are consistent with previous findings.…”

Section: Discussionmentioning

confidence: 98%

Diagnostic and predictive significance of serum microRNA-7 in esophageal squamous cell carcinoma

Wang

et al. 2015

Oncology Reports

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MicroRNA-138 suppresses invasion and promotes apoptosis in head and neck squamous cell carcinoma cell lines

Cited by 190 publications

References 49 publications

MicroRNA‑138 targets SP1 to inhibit the proliferation, migration and invasion of hepatocellular carcinoma cells

MicroRNA‑138 targets SP1 to inhibit the proliferation, migration and invasion of hepatocellular carcinoma cells

Inhibition of ABCB1 Overcomes Cancer Stem Cell–like Properties and Acquired Resistance to MET Inhibitors in Non–Small Cell Lung Cancer

Diagnostic and predictive significance of serum microRNA-7 in esophageal squamous cell carcinoma

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