MiR-138: A promising therapeutic target for cancer

Sha, Huanhuan; Wang, Dandan; Chen, Dan; Siwen, Liu; Wang, Zhen; Yan, Dali; Dong, Shuchen; Feng, Jifeng

doi:10.1177/1010428317697575

Cited by 76 publications

(60 citation statements)

References 90 publications

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“…It has been reported that important signaling pathways in CRC, such as the Wnt/β-catenin, RAS, p53, TGF-β, NF-kB pathways, are regulated by miRNAs [21–23]. A number of studies have demonstrated that miR-138 regulates various molecular pathways and is associated with initiation and progression of cancer, and thus is considered as a potential tumor suppressor [24]. As reported by Jiang et al[25], ectopic transfection of miR-138 contributed to the reduced migration and invasion in oral tongue squamous cell carcinoma by targeting RhoC and ROCK2, which are involved in the remodeling of cellular cytoskeleton.…”

Section: Discussionmentioning

confidence: 99%

“…In this study, we found that miR-138 was up-regulated by ANGPTL1, but the mechanism of its biogenesis remains unexplored. As reported, epigenetic and transcription factors, as well as many other molecules, are correlated with miR-138 expression [24]. For example, miR-138 expression can be decreased by methylation of its DNA [27] and up-regulated by a histone deacetylase inhibitor [28] and overexpression of P 19 H-Ras [29].…”

Section: Discussionmentioning

confidence: 99%

“…With respect to the potential targets of miR-138, EMT, the TGF-β pathway, the RhoC-Erk-MMP-2/9 pathway, and the cofilin pathway have been identified to participate in the reduced migratory and invasive activity induced by miR-138 [24]. Specifically, miR-138 overexpression inhibits EMT process by targeting Vimentin and EZH2, thus reducing breast cancer invasion [30].…”

Section: Discussionmentioning

confidence: 99%

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ANGPTL1 attenuates colorectal cancer metastasis by up-regulating microRNA-138

Chen

Xiao

et al. 2017

J Exp Clin Cancer Res

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BackgroundAngiopoietin-like protein 1 (ANGPTL1) has been reported to suppress migration and invasion in lung and breast cancer, acting as a novel tumor suppressor candidate. Nevertheless, its effects on colorectal cancer (CRC) remain poorly defined. In this study, we aim to demonstrate the biological function of ANGPTL1 in CRC cells.MethodsWe explored ANGPTL1 mRNA expression in human CRC tissues and its association with prognosis. CRC cell lines overexpressing ANGPTL1 or with ANGPTL1 knocked down were constructed and analyzed for changes in proliferation, colony formation, migration and invasion. ANGPTL1-regulated microRNAs were analyzed, and microRNA inhibitor and mimics were used to explore the role of microRNA in ANGPTL1-associated biological function.ResultsANGPTL1 mRNA expression was down-regulated in CRC tissues, and high ANGPTL1 expression predicted better survival in CRC patients. ANGPTL1 overexpression resulted in suppressed migration and invasion in vitro, and it prolonged overall survival in mouse models. By contrast, its down-regulation enhanced migration and invasion of CRC cells. MicroRNA-138 expression was positively correlated with ANGPTL1 mRNA level in CRC tissues and up-regulated by ANGPTL1 in CRC cells. In addition, the microRNA-138 inhibitor or mimics could reverse or promote the ANGPTL1-mediated inhibition of the migratory capacity of CRC cells, respectively.ConclusionsThis study is the first to demonstrate the biological function of ANGPTL1 in CRC cells. ANGPTL1 expression was down-regulated in CRC tissues and inversely correlated with poor survival. ANGPTL1 repressed migration and invasion of CRC cells, and microRNA-138 was involved in this process.Electronic supplementary materialThe online version of this article (doi:10.1186/s13046-017-0548-7) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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ANGPTL1 attenuates colorectal cancer metastasis by up-regulating microRNA-138

Chen

Xiao

et al. 2017

J Exp Clin Cancer Res

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“…A growing number of studies have confirmed that miRNAs play essential roles in the diagnosis, development, prognosis, and treatment of a variety of tumors. miRs will become potential therapeutic targets, anticancer agents, and biomarkers for the treatment of cancer and bring novel guidance in molecular targeting treatment of cancers in the future . Approximately about 85% of lung diseases are associated with non‐small cell lung cancer (NSCLC), it is one of the most leading causes of cancer mortality and the most prevalent cancers.…”

Section: Introductionmentioning

confidence: 99%

“…miRs will become potential therapeutic targets, anticancer agents, and biomarkers for the treatment of cancer and bring novel guidance in molecular targeting treatment of cancers in the future. [80][81][82][83] Approximately about 85% of lung diseases are associated with non-small cell lung cancer (NSCLC), it is one of the most leading causes of cancer mortality and the most prevalent cancers. Its development and occurrence are closely associated with tumor angiogenesis.…”

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confidence: 99%

MicroRNAs play an essential role in autophagy regulation in various disease phenotypes

et al. 2019

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Autophagy is a highly conserved catabolic process and fundamental biological process in eukaryotic cells. It recycles intracellular components to provide nutrients during starvation and maintains quality control of organelles and proteins. In addition, autophagy is a well‐organized homeostatic cellular process that is responsible for the removal of damaged organelles and intracellular pathogens. Moreover, it also modulates the innate and adaptive immune systems. Micro ribonucleic acids (microRNAs) are a mature class of post‐transcriptional modulators that are widely expressed in tissues and organs. And, it can suppress gene expression by targeting messenger RNAs for translational repression or, at a lesser extent, degradation. Research indicates that microRNAs regulate autophagy through different pathways, playing an essential role in the treatment of various diseases. It is an important regulator of fundamental cellular processes such as proliferation, autophagy, and cell apoptosis. In this review article, we first review the current knowledge of autophagy and the function of microRNAs. Then, we summarize the mechanism of autophagy and the signaling pathways related to autophagy by citing at least the main proteins involved in the different phases of the process. Second, we introduce other members of RNA and report some examples in various pathologies. Finally, we review the current literature regarding microRNA‐based therapies for cancer, atherosclerosis, cardiac disease, tuberculosis, and viral diseases. MicroRNAs can cause autophagy upregulation or downregulation by targeting genes or affecting autophagy‐related signaling pathways. Therefore, the microRNAs have a huge potential in autophagy regulation, and it is the function as diagnostic and prognostic markers.

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MicroRNA‐138 Inhibits Osteogenic Differentiation and Mineralization of Human Dedifferentiated Chondrocytes by Regulating RhoC and the Actin Cytoskeleton

et al. 2018

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MicroRNAs (miRNAs) are known to play critical roles in many cellular processes including those regulating skeletal development and homeostasis. A previous study from our group identified differentially expressed miRNAs in the developing human growth plate. Among those more highly expressed in hypertrophic chondrocytes compared to progenitor chondrocytes was miR‐138, therefore suggesting a possible role for this miRNA in regulating chondrogenesis and/or endochondral ossification. The goal of this study was to determine the function of miR‐ 138 in regulating osteogenesis by using human osteoarthritic dedifferentiated chondrocytes (DDCs) as source of inducible cells. We show that over‐expression of miR‐138 inhibited osteogenic differentiation of DDCs in vitro. Moreover, cell shape was altered and cell proliferation and possibly migration was also suppressed by miR‐138. Given alterations in cell shape, closer analysis revealed that F‐actin polymerization was also inhibited by miR‐138. Computational approaches showed that the small GTPase, RhoC, is a potential miR‐138 target gene. We pursued RhoC further given its function in regulating cell proliferation and migration in cancer cells. Indeed, miR‐138 over‐expression in DDCs resulted in decreased RhoC protein levels. A series of rescue experiments showed that RhoC over‐expression could attenuate the inhibitory actions of miR‐138 on DDC proliferation, F‐actin polymerization and osteogenic differentiation. Bone formation was also found to be enhanced within human demineralized bone scaffolds seeded with DDCs expressing both miR‐138 and RhoC. In conclusion, we have discovered a new mechanism in DDCs whereby miR‐138 functions to suppress RhoC which subsequently inhibits proliferation, F‐actin polymerization and osteogenic differentiation. To date, there are no published reports on the importance of RhoC in regulating osteogenesis. This opens up new avenues of research involving miR‐138 and RhoC pathways to better understand mechanisms regulating bone formation in addition to the potential use of DDCs as a cell source for bone tissue engineering. © 2018 The Authors. JBMR Plus is published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research.

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MiR-138: A promising therapeutic target for cancer

Cited by 76 publications

References 90 publications

ANGPTL1 attenuates colorectal cancer metastasis by up-regulating microRNA-138

ANGPTL1 attenuates colorectal cancer metastasis by up-regulating microRNA-138

MicroRNAs play an essential role in autophagy regulation in various disease phenotypes

MicroRNA‐138 Inhibits Osteogenic Differentiation and Mineralization of Human Dedifferentiated Chondrocytes by Regulating RhoC and the Actin Cytoskeleton

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