miR‑138 modulates prostate cancer cell invasion and migration via Wnt/β‑catenin pathway

Yu, Zhongwei; Wang, Zulin; Li, Feng; Yang, Jiping; Tang, Laikun

doi:10.3892/mmr.2017.8273

Cited by 16 publications

(18 citation statements)

References 35 publications

(33 reference statements)

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“…However, in these in vitro scratch assays, we acknowledge that part of the reason we observed lower cell numbers in the scratched area may also be based on the inhibitory effects on cell proliferation. However, there are a number of studies reporting inhibitory effects of miR‐138 on cell migration and invasion in the cancer field, some of which are referenced here . Of these studies, Yu and colleagues recently reported that miR‐138 modulates prostate cancer cell migration and invasion by negatively regulating the Wnt/β‐catenin pathway, a pathway that is also well‐known to be important for osteoblast differentiation .…”

Section: Discussionmentioning

confidence: 99%

“…However, there are a number of studies reporting inhibitory effects of miR‐138 on cell migration and invasion in the cancer field, some of which are referenced here . Of these studies, Yu and colleagues recently reported that miR‐138 modulates prostate cancer cell migration and invasion by negatively regulating the Wnt/β‐catenin pathway, a pathway that is also well‐known to be important for osteoblast differentiation . Furthermore, cell invasion was found to be inhibited by the ability of miR‐138 to target FAK .…”

Section: Discussionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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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“…Multiple studies have demonstrated that miRNAs are involved in the regulation of various biological processes such as cancer invasion or migration by targeting the majority of protein-coding genes (11,12). Accumulating data has suggested that the abnormal expression of miRNAs was implicated in the progression of PCa through numerous signaling pathways, including Notch and HIF-1α pathways (13)(14)(15)(16). Hence, it is necessary to determine the functions of miRNAs in PCa, which may reveal a novel mechanism of PCa progression.…”

Section: Terf1 Downregulation Promotes the Migration And Invasion Of mentioning

confidence: 99%

TERF1 downregulation promotes the migration and invasion of the PC3 prostate cancer cell line as a target of miR‑155

Chen

He²,

Liang

et al. 2020

Mol Med Rep

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Telomeric repeat binding factor 1 (TerF1) has been identified as a tumor suppressor gene in numerous types of human cancer. However, the expression of TERF1 and its mechanism in prostate cancer (PCa) remains unclear. The present study aimed to explore the expression and functions of TERF1 in PCa. The UALCAN database was used to analyze the differential expression of TERF1 between normal prostate tissue and primary PCa tissue. Cell apoptosis was analyzed by Annexin V/propidium iodide staining, and wound healing and Transwell assays were used to detect the cell migration and invasion abilities, respectively. The cell viability was analyzed using an MTT assay. Reverse transcription-quantitative PCR and western blotting were used to analyze the mRNA and protein expression levels, respectively, of epithelial-mesenchymal transition (EMT) markers following TERF1 knockdown in the PC3 cell line. A dual luciferase reporter assay was used to verify the association between TERF1 and microRNA (miR)-155 predicted by bioinformatics analysis. Rescue experiments were performed to determine the role of the miR-155/TERF1 axis in regulating the cellular behaviors of PCa. The results demonstrated that the expression levels of TERF1 in the primary prostate tumors were significantly downregulated compared with in prostate normal tissue. TERF1 silencing was discovered to significantly promote cell viability, migration and invasion, while suppressing cell apoptosis. The impact of TERF1 on PC3 cells was suggested to occur through the EMT pathway. TERF1 was confirmed to be the direct target of miR-155. The overexpression of miR-155 promoted the viability, migration and invasion, while suppressing the apoptosis of the PC3 cell line, while the knockdown of miR-155 in PC3 cells achieved the opposite trends. In addition, TERF1 overexpression reversed the promotive effects of upregulated miR-155 expression levels on the migration and apoptosis of PC3 cells. On the contrary, the knockdown of TERF1 reversed the migration and apoptosis abilities of the downregulated miR-155 expression levels on the cellular behaviors of PC3 cells. In conclusion, TERF1, as a direct target of miR-155, was discovered to be significantly downregulated in PCa, which was suggested to promote the migration and invasion of PCa via the EMT pathway.

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“…miR-1247-5p functions as a tumor suppressor by activating Wnt3 (18). It was also demonstrated that miR-138 modulates prostate cancer cell invasion and migration via the Wnt/β-catenin pathway (19). In the present study, the association of miR-2053 with the PI3K/AKT/mTOR and Wnt/β-catenin pathways in HCC cells was explored.…”

Section: Introductionmentioning

confidence: 84%

MicroRNA‑2053 overexpression inhibits the development and progression of hepatocellular carcinoma

Song

Zhao

et al. 2019

Oncol Lett

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MicroRNAs (miRNAs) represent a class of small RNAs that participate in the regulation of tumor progression. However, the identification of functional miRNAs in tumors has not been thoroughly elucidated. In the present study we aim to investigate the impact of altered miR-2053 expression in hepatocellular carcinoma (HCC) cells. The results of the present study demonstrated that miR-2053 overexpression inhibited cell proliferation, migration and invasion, and promoted apoptosis in a HCC cell line, while miR-2053 knockdown induced the opposite cellular phenotypic changes. Mechanistically, it was found that overexpression of miR-2053 resulted in the downregulation of the phosphoinositide 3-kinase (PI3K) and Wnt/β-catenin signaling pathways, which are aberrantly expressed in HCC. Collectively, the results indicate that miR-2053 serves as a tumor suppressor with a crucial role in inhibiting the proliferation, migration and invasion of HCC via targeting the PI3K and Wnt/β-catenin signaling pathways. These data indicate a potential application of miR-2053 in cancer therapy.

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miR‑138 modulates prostate cancer cell invasion and migration via Wnt/β‑catenin pathway

Cited by 16 publications

References 35 publications

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

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

TERF1 downregulation promotes the migration and invasion of the PC3 prostate cancer cell line as a target of miR‑155

MicroRNA‑2053 overexpression inhibits the development and progression of hepatocellular carcinoma

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