miR‑124 regulates STAT3‑mediated cell proliferation, migration and apoptosis in bladder cancer

Wang, Shengxing; Wu, Gang; Han, Yinan; Song, Peng; Jinhuo, Chen; Wu, Yaoxi; Yang, Jie; Liang, Ping

doi:10.3892/ol.2018.9341

Cited by 15 publications

(15 citation statements)

References 36 publications

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“…A report stated that the expression of miR‐124 could inhibit the growth of human epithelial ovarian cancer cell xenografts . Wang et al demonstrated that miR‐124 could regulate STAT3 protein expression and have a tumor suppressor function in proliferation and apoptosis in bladder cancer cell lines (T24) through the miR‐124/STAT3 signaling pathway . Another study on the same bladder cancer cell line showed that miR‐124 controlled the target gene Caveolin 1 (CAV1) and played a suppressive role in the proliferation, migration, and invasion of bladder cancer .…”

Section: Mir‐124 and Other Malignant Tumorsmentioning

confidence: 99%

“…112 Wang et al demonstrated that miR-124 could regulate STAT3 protein expression and have a tumor suppressor function in proliferation and apoptosis in bladder cancer cell lines (T24) through the miR-124/STAT3 signaling pathway. 113 Another study on the same bladder cancer cell line showed that miR-124 controlled the target gene Caveolin 1 (CAV1) and played a suppressive role in the proliferation, migration, and invasion of bladder cancer. 114 Additionally, the lncRNA MALAT1 may function as a ceRNA to sponge miR-124 by modulating the depression of foxq1 at posttranscriptional levels and promoting bladder transitional cell carcinoma cell (BIU-87) proliferation, migration, and invasion.…”

Section: Malignant Tumorsmentioning

confidence: 99%

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MicroRNA‐124: An emerging therapeutic target in cancer

et al. 2019

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MicroRNAs (miRNAs) are noncoding single‐stranded RNAs, approximately 20‐24 nucleotides in length, known as powerful posttranscriptional regulators. miRNAs play important regulatory roles in cellular processes by changing messenger RNA expression and are widely involved in human diseases, including tumors. It has been reported in the literature that miRNAs have a precise role in cell proliferation, programmed cell death, differentiation, and expression of coding genes. MicroRNA‐124 (miR‐124) has reduced exparession in various human neoplasms and is believed to be related to the occurrence, development, and prognosis of malignant tumors. In our review, we focus on the specific molecular functions of miR‐124 and the downstream gene targets in major cancers, which provide preclinical evidence for the treatment of human cancer. Although some obstacles exist, miR‐124 is still attracting intensive research focus as a promising and effective anticancer weapon.

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Section: Mir‐124 and Other Malignant Tumorsmentioning

confidence: 99%

Section: Malignant Tumorsmentioning

confidence: 99%

MicroRNA‐124: An emerging therapeutic target in cancer

et al. 2019

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“…miR-124-3p.1 can inhibit cell proliferation and suppress tumor growth in colorectal cancer, bladder cancer, and renal cell carcinoma. [25][26][27] Furthermore, miR-124-3p.1 has been shown to reduce drug resistance in some cancers. 28,29 However, the mechanisms underlying these effects remain unclear.…”

Section: Introductionmentioning

confidence: 99%

<p>MiR-124-3p.1 Sensitizes Ovarian Cancer Cells to Mitochondrial Apoptosis Induced by Carboplatin</p>

Deng¹,

Chen²,

Liu³

et al. 2020

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Background: Carboplatin is a platinum-based chemotherapeutic drug that is commonly used as a treatment for ovarian cancer. However, high doses and repeated use of carboplatin usually reduce the sensitivity of cancer cells to the drug. There is an urgent need to develop strategies to increase the sensitivity of ovarian cancer cells to carboplatin. Materials and Methods: Quantitative reverse-transcriptase real-time PCR was used to detect miR-124-3p.1 levels in ovarian cancer tissues and cell lines. Transfection with miR-124-3p.1 and caveolin-1 (CAV1) was used for gain-of-function experiments. Western blot and immunoprecipitation assays were performed to evaluate the expression and function of CAV1, AKT, Bad, and Bcl-xl. Flow cytometry analysis was used to measure the apoptosis rates of SKOV3 and A2780 cells. Results: Expression levels of miR-124-3p.1 were decreased in ovarian cancer tissues and cell lines. Furthermore, overexpression of miR-124-3p.1 enhanced carboplatin-induced apoptotic cell death of ovarian cancer cell lines. Regarding the mechanism of this effect, we showed that CAV1 was the target of miR-124-3p.1 in ovarian cancer. Overexpression of miR-124-3p.1 suppressed the expression of CAV1, thereby reducing the activation of AKT and phosphorylation of Bad. As a result, the function of Bcl-xl was inhibited and carboplatininduced mitochondrial apoptosis was enhanced. Conclusion: miR-124-3p.1 sensitizes carboplatin-induced mitochondrial apoptosis through suppression of CAV1 in ovarian cancer. Increasing miR-124-3p.1 expression may represent a novel strategy to improve carboplatin sensitivity in ovarian cancer.

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“…A study has found that miR-124 played an important role in the occurrence and development of BC. Wang’s study found that miR-124 could regulate STAT3-mediated cell migration and apoptosis in bladder cancer 44. It has also been found that miR-124 can regulate BC cell apoptosis or metastasis by targeting CAV1 or DNMT3B 45,46.…”

Section: Discussionmentioning

confidence: 99%

<p>The functions of microRNA-124 on bladder cancer</p>

Cao¹,

Xu²,

Zhao³

et al. 2019

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Background: To detect the expression of miR-124 in bladder cancer (BC) cell lines and tissue specimens and to analyze its association with the growth of the BC cells. Methods: Quantitative real-time polymerase chain reaction (qPCR) was applied to examine the expression of miR-124 in BC cell lines and tissues. The function of miR-124 in modulating cell proliferation was assessed in BC cells with miRNA-124 overexpression; the cell viability was identified by Cell Count Kit-8; flow cytometry was employed to detect the cell cycle; the expressions of E2F3, cyclin-dependent kinase 4 (CDK4), Ki-67 and vascular endothelial growth factor (VEGF) were tested by qPCR and Western blot; angiogenesis experiment was performed to analysis changes in angiogenesis rate; and bioinformatics prediction and dual luciferase reporter system were employed to identify the target of miR-124. Results: Survival curve data showed that the expression of MicroRNA-124 was positively correlated with survival. MicroRNA-124 expression was significantly decreased in BC cell lines and tissues. Bioinformatics prediction and dual luciferase reporter system verified CDK4 as a direct target of miR-124, which regulated the proliferation of BC cells by directly inhibiting CDK4. BC cells over-expressing miR-124 showed significantly inhibited cell viability, decreased angiogenesis rate, prevented cell proliferation and diminished the expression of E2F3, CDK4, Ki-67 and VEGF. All of these changes were reversed by over-expressing CDK4. Conclusion: MicroRNA-124 suppressed the proliferation of CRC cells by directly targeting CDK4, which provides a target for improving the therapeutic effect of BC.

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miR‑124 regulates STAT3‑mediated cell proliferation, migration and apoptosis in bladder cancer

Cited by 15 publications

References 36 publications

MicroRNA‐124: An emerging therapeutic target in cancer

MicroRNA‐124: An emerging therapeutic target in cancer

<p>MiR-124-3p.1 Sensitizes Ovarian Cancer Cells to Mitochondrial Apoptosis Induced by Carboplatin</p>

<p>The functions of microRNA-124 on bladder cancer</p>

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