MiR‑506 inhibits cell proliferation, invasion, migration and epithelial‑to‑mesenchymal transition through targeting RWDD4 in human bladder cancer

Hou, Yi

doi:10.3892/ol.2018.9594

Cited by 11 publications

(14 citation statements)

References 26 publications

(25 reference statements)

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“…More than 1/3 of all human genes are controlled by miRNA . Increasing evidence has suggested the important role of miRs in the progression of BC . For instance, miR‐206 is reported to be a tumor suppressor in BC via inhibiting the expression of YRDC .…”

Section: Introductionmentioning

confidence: 99%

“…For instance, miR‐206 is reported to be a tumor suppressor in BC via inhibiting the expression of YRDC . And miR‐506 is shown to suppress BC cell proliferation, invasion, and migration via targeting RWDD4 . Abnormal expression of miR‐323a has been widely identified in various tumors, including prostate cancer and glioma .…”

Section: Introductionmentioning

confidence: 99%

“…7 Increasing evidence has suggested the important role of miRs in the progression of BC. 8,9 For instance, miR-206 is reported to be a tumor suppressor in BC via inhibiting the expression of YRDC. 8 And miR-506 is shown to suppress BC cell proliferation, invasion, and migration via targeting RWDD4.…”

Section: Introductionmentioning

confidence: 99%

“…8 And miR-506 is shown to suppress BC cell proliferation, invasion, and migration via targeting RWDD4. 9 Abnormal expression of miR-323a has been widely identified in various tumors, including prostate cancer and glioma. 10,11 For instance, higher levels of miR-323 are shown in prostate cancer and it is found to increase the vessel formation via targeting adiponectin receptor.…”

Section: Introductionmentioning

confidence: 99%

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Increased miR‐323a induces bladder cancer cell apoptosis by suppressing c‐Met

Qiu

Zeng

Fang

et al. 2019

The Kaohsiung J of Med Scie

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The current study aimed to evaluate the expression and role of miR‐323a in the progression of bladder cancer (BC), thereby providing a theoretical basis and potential therapy methods for BC patients. Our data showed that miR‐323a levels were significantly reduced in BC tissues compared with those of non‐cancerous tissues. Meanwhile, miR‐323a was significantly decreased in human BC cell lines (T24, J82, TCCSUP, RT‐112) than that in human normal bladder epithelial cell line SV‐HUC‐1. Furthermore, inhibition of miR‐323a markedly enhanced the migration and invasive capacity of T24 and TCCSUP cells. Moreover, overexpression of miR‐323a significantly prompted the apoptosis of BC cells. Dual luciferase reporter assay and western blot analysis confirmed that c‐Met was a target gene of miR‐323a. More importantly, upregulation of c‐Met significantly prompted BC cell proliferation mainly as a result of the enhanced level of phosphorylation of AKT. This effect could be abolished when c‐Met was silenced in BC cells. In summary, reduced miR‐323a expression in BC contributed to enhanced BC cell proliferation and migration mainly by targeting c‐Met.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Increased miR‐323a induces bladder cancer cell apoptosis by suppressing c‐Met

Qiu

Zeng

Fang

et al. 2019

The Kaohsiung J of Med Scie

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“…Several studies have shown that among the potential causes for BC, there are a variety of molecular factors such as noncoding RNAs (10)(11)(12)(13)(14)(15). Included in the latter are microRNAs (miRNAs), a class of small noncoding RNAs that regulate gene protein expression by repressing protein translation or by affecting mRNA stability through binding to its specific target sequences.…”

mentioning

confidence: 99%

Inhibition of UBE2N‐dependent CDK6 protein degradation by miR‐934 promotes human bladder cancer cell growth

Huang¹,

Ren²,

Lin

et al. 2019

FASEB j.

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Because bladder cancer (BC) is one of the most common malignant cancers of the urinary system, identification of BC cell growth‐associated effectors is of great significance. Cyclin‐dependent kinase (CDK)6 is a member of the CDK family of cell cycle‐related proteins and plays an important role in cancer cell growth. This is borne out by the fact that a CDK6 inhibitor had been approved to treat several types of cancers. Nevertheless, underlying molecular mechanisms concerning how to regulate CDK6 expression in BC remains unclear. In the present study, it was observed that miR‐934 was much higher in human BCs and human BC cell lines as well. The results also revealed that miR‐934 inhibition dramatically decreased human BC cell monolayer growth in vitro and xenograft tumor growth in vivo; the outcomes were accompanied by CDK6 protein down‐regulation and G0‐G1 cell cycle arrest. Moreover, overexpression of CDK6 reversed the inhibition of BC cell growth induced by miR‐934. Further studies showed that miR‐934 binds to a 3'‐UTR of ubiquitin‐conjugating enzyme 2N (ube2n) mRNA, down‐regulated UBE2N protein expression; this, in turn, attenuated CDK6 protein degradation and led to CDK6 protein accumulation as well as the promotion of BC tumor growth. Collectively, this study not only establishes a novel regulatory axis of miR‐934/UBE2N of CDK6 but also provides data suggesting that miR‐934 and UBE2N may be potentially promising targets for therapeutic strategies against BC.—Yan, H., Ren, S., Lin, Q., Yu, Y., Chen, C., Hua, X., Jin, H., Lu, Y., Zhang, H., Xie, Q., Huang, C., Huang, H. Inhibition of UBE2N‐dependent CDK6 protein degradation by miR‐934 promotes human bladder cancer cell growth. FASEB J. 33, 12112‐12123 (2019). http://www.fasebj.org

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