Micro<scp>RNA</scp>‐137 suppresses tongue squamous carcinoma cell proliferation, migration and invasion

Sun, Lingyun; Jin, Liang; Wang, Qibao; Li, Zhaoyuan; Du, Yi; Xu, Xin

doi:10.1111/cpr.12287

Cited by 48 publications

(42 citation statements)

References 61 publications

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“…miR-137 hypermethylation leads to its inhibition in many tumors, such as colorectal cancer, pancreatic cancer, and endometrial cancer [29][30][31] . Functional analysis has indicated that miR-137 can inhibit cell proliferation, cell cycle arrest and apoptosis, cell migration and invasion, and affect chemoresistance [32][33][34][35][36] . For example, miR-137 overexpression sensitized resistant colon cancer cells to oxaliplatin 20 .…”

Section: Discussionmentioning

confidence: 99%

miR-137 alleviates doxorubicin resistance in breast cancer through inhibition of epithelial-mesenchymal transition by targeting DUSP4

et al. 2019

Cell Death Dis

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Acquired resistance to chemotherapy is a major obstacle in breast cancer (BC) treatment. Accumulated evidence has uncovered that microRNAs (miRNAs) are vital regulators of chemoresistance in cancer. Growing studies reveal that miR-137 acts as a suppressor in tumor progression. However, it remains obscure the role of miR-137 in modulating the sensitivity of BC cells to doxorubicin (DOX). In this study, we demonstrate that miR-137 exerts a significant effect on repressing the development of chemoresistance of BC cells in response to DOX via attenuating epithelialmesenchymal transition (EMT) of tumor cells in vitro and in vivo. MiR-137 overexpression dramatically elevated the sensitivity of BC cells to DOX as well as impaired the DOX-promoted EMT of tumor cells. Mechanistically, miR-137 directly targeted dual-specificity phosphatase 4 (DUSP4) to impact on the EMT and chemoresistance of BC cells upon DOX treatment. Consistently, decreased DUSP4 efficiently enhanced the sensitivity of BC cells to DOX while overexpressed DUSP4 significantly diminished the beneficial effect of miR-137 on BC cells chemoresistance. Moreover, the increased miR-137 heightened the sensitivity of BC cells-derived tumors to DOX through targeting DUSP4 in vivo. Together, our results provide a novel insight into the DOX resistance of BC cells and miR-137 may serve as a new promising therapeutic target for overcoming chemoresistance in BC.

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Section: Discussionmentioning

confidence: 99%

miR-137 alleviates doxorubicin resistance in breast cancer through inhibition of epithelial-mesenchymal transition by targeting DUSP4

et al. 2019

Cell Death Dis

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“…MicroRNAs (miRNAs) are endogenous, short (~22 nucleotide), noncoding, single‐stranded RNAs that can regulate translational inhibition or mRNA degradation by binding to the 3′ untranslated regions (3′‐UTRs) of some specific mRNAs . Studies have shown that miRNAs participate in a range of pathological and physiological processes, including cell proliferation, differentiation, apoptosis, organ development, and tumor oncogenesis . In particular, numerous studies have published that miRNAs play critical roles in osteogenic differentiation .…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐3064‐3p regulates the differentiation of cementoblasts through targeting DKK1

Wang

Liao

Sun

et al. 2018

J of Periodontal Research

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“…Increasingly, evidence has suggested that Sp1 may be involved in a variety of cellular processes, including cell growth, survival, differentiation, tumor development and tumor progression (35)(36)(37)(38). miRs, which regulate the expression of their target genes by base pairing with seed sequences in the 3'-UTR of mRNAs, have been shown to regulate the expression of Sp1 (39,40). In a previous study, miR-22 was reported to be downregulated in GC and inhibited cell proliferation, migration and invasion by targeting Sp1 (41).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-429 inhibits gastric cancer migration and invasion through the downregulation of specificity protein 1

Yang

Liu

et al. 2017

Oncology Letters

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Abstract. microRNAs (miRs) have been reported to have an important role in tumorigenesis and tumor progression. Although miR-429 has been shown to be downregulated in gastric cancer (GC), the function of miR-429 in the metastasis of GC has yet to be investigated. In the present study, GC cells were transfected with miR-429, and reverse transcription-quantitative polymerase chain reaction, cell migration assays, cell invasion assays, western blot analysis and luciferase assays were conducted to investigate the role of miR-429 in GC cells. It was demonstrated that miR-429 expression was markedly increased following transfection of the cells with miR-429. Furthermore, miR-429 was shown to inhibit the migration and invasion of GC cell lines. In addition, this study provided evidence that miR-429 directly targets specificity protein 1 in GC cells. The results of the present study may enhance current knowledge regarding the molecular basis of cancer metastasis and provide a potential therapeutic strategy for GC.

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MicroRNA‐137 suppresses tongue squamous carcinoma cell proliferation, migration and invasion

Abstract: These results indicate that miR-137 acted as a tumour suppressor in TSCC by targeting SP1.

Cited by 48 publications

References 61 publications

miR-137 alleviates doxorubicin resistance in breast cancer through inhibition of epithelial-mesenchymal transition by targeting DUSP4

miR-137 alleviates doxorubicin resistance in breast cancer through inhibition of epithelial-mesenchymal transition by targeting DUSP4

MicroRNA‐3064‐3p regulates the differentiation of cementoblasts through targeting DKK1

MicroRNA-429 inhibits gastric cancer migration and invasion through the downregulation of specificity protein 1

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