CCND1, NOP14 and DNMT3B are involved in miR‐502‐5p–mediated inhibition of cell migration and proliferation in bladder cancer

Ying, Yufan; Li, Jiangfeng; Xie, Haiyun; Yan, Huaqing; Jin, Ke; He, Liujia; Ma, Xueyou; Wu, Jian; Xu, Xin; Fang, Jiajie; Wang, Xiao; Zheng, Xiangyi; Liu, Ben; Xie, Liping

doi:10.1111/cpr.12751

Cited by 47 publications

(32 citation statements)

References 39 publications

(82 reference statements)

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“…On the other hand, some miRNAs have been documented to exert suppressing functions in BCs. miR-502-5p, for example, has been recently found to suppress the malignant behaviors of BCs cells through the different miRNA targets including CCND1, NOP14 and DNMT3B [21]. Similar trends have also been previously in miR-124-3p [22] and miR-203a [23].…”

Section: Discussionsupporting

confidence: 68%

MicroRNA-381 inhibits bladder cancer pathogenesis through directly controlling BMI1 and triggering the Rho/ROCK signaling pathway defect

Chen

Liu

Cao

et al. 2020

Preprint

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Background Emerging evidence has noted the important participation of microRNAs (miRNAs) in several human diseases including cancer control. This research was launched to probe the function of miR-381 in bladder cancer (BCs) progression. Methods Aberrantly expressed miRNAs in BCs tissues were analyzed using miRNA microarrays. miR-381 expression in the bladder and paired tumor tissues, and in BCs and normal cell lines was determined. The target relationship between miR-381 and BMI1 was predicted online and validated through a luciferase assay. Gain-of-functions of miR-381 and BMI1 were performed to identify their functions on BCs cell behaviors as well as tumor growth in vivo. Results miR-381 was poor regulated in BCs tissues and cells. A higher miR-381 level indicates a better prognosis of patients with BCs. Artificial up-regulation of miR-381 inhibited proliferation, invasion, migration, resistance to apoptosis, and tumor formation ability of BCs cells. miR-381 directly binds to BMI1 expression. Overexpression of BMI1 partially blocked the tumor suppressing roles of miR-381 in cell malignancy and tumor growth. In addition, miR-381 led to decreased RhoA phosphorylation and ROCK2 activation, which were also reversed by BMI1. Conclusion The study evidenced that miR-381 may act as a beneficiary biomarker in BCs patients. Up-regulation of miR-381 could suppress BCs development both in vivo and in vitro through BMI1 down-regulation and the Rho/ROCK inactivation.

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Section: Discussionsupporting

confidence: 68%

MicroRNA-381 inhibits bladder cancer pathogenesis through directly controlling BMI1 and triggering the Rho/ROCK signaling pathway defect

Chen

Liu

Cao

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…On the other hand, some miRNAs have been documented to exert suppressing functions in BCa. miR-502-5p, for example, has been recently found to suppress the malignant behaviors of BCa cells through the different miRNA targets including CCND1, NOP14 and DNMT3B [ 23 ]. Similar trends have also been seen in miR-124-3p [ 24 ] and miR-203a [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

Role of microRNA-381 in bladder cancer growth and metastasis with the involvement of BMI1 and the Rho/ROCK axis

et al. 2021

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Background Emerging evidence has noted the important participation of microRNAs (miRNAs) in several human diseases including cancer. This research was launched to probe the function of miR-381 in bladder cancer (BCa) progression. Methods Twenty-eight patients with primary BCa were included in this study. Cancer tissues and the adjacent normal tissues were obtained. Aberrantly expressed miRNAs in BCa tissues were analyzed using miRNA microarrays. miR-381 expression in the bladder and paired tumor tissues, and in BCa and normal cell lines was determined. The target relationship between miR-381 and BMI1 was predicted online and validated through a luciferase assay. Gain-of-functions of miR-381 and BMI1 were performed to identify their functions on BCa cell behaviors as well as tumor growth in vivo. The involvement of the Rho/ROCK signaling was identified. Results miR-381 was poor regulated in BCa tissues and cells (all p < 0.05). A higher miR-381 level indicated a better prognosis of patients with BCa. Artificial up-regulation of miR-381 inhibited proliferation, invasion, migration, resistance to apoptosis, and tumor formation ability of BCa T24 and RT4 cells (all p < 0.05). miR-381 was found to directly bind to BMI1 and was negatively correlated with BMI1 expression. Overexpression of BMI1 partially blocked the tumor suppressing roles of miR-381 in cell malignancy and tumor growth (all p < 0.05). In addition, miR-381 led to decreased RhoA phosphorylation and ROCK2 activation, which were also reversed by BMI1 (all p < 0.05). Artificial inhibition of the Rho/ROCK signaling blocked the functions of BMI1 in cell growth and metastasis (all p < 0.05). Conclusion The study evidenced that miR-381 may act as a beneficiary biomarker in BCa patients. Up-regulation of miR-381 suppresses BCa development both in vivo and in vitro through BMI1 down-regulation and the Rho/ROCK inactivation.

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“…Results showed that hsa_circ_0000231 was a sponge of miR-502-5p. It has been illustrated that miR-502-5p was indicated to inhibit cell proliferation and metastasis in bladder cancer and gastric cancer [12,13]. In breast cancer, miR-502-5p was downregulated and suppressed cell proliferation, whereas promoted cell apoptosis [26].…”

Section: Discussionmentioning

confidence: 99%

“…MiR-502-5p is indicated to participate in cancer progression [ 9 – 11 ]. For example, miR-502-5p overexpression represses cell metastasis in bladder cancer [ 12 ]. MiR-502-5p is also indicated to regulate the tumorigenesis and metastasis of gastric cancer [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Hsa_circ_0000231 knockdown inhibits the glycolysis and progression of colorectal cancer cells by regulating miR-502-5p/MYO6 axis

Liu

et al. 2020

World J Surg Onc

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Background Colorectal cancer (CRC) poses a heavy threat to human health owing to its high incidence and mortality. Circular RNAs (circRNAs) were investigated to participate in the progression of CRC, whereas there was no revenant data on the CRC process regulated by hsa_circ_0000231. This study aimed to explore the effects of hsa_circ_0000231 on CRC progression and underneath regulatory mechanism. Methods The expression levels of hsa_circ_0000231, miR-502-5p, and Myosin VI (MYO6) mRNA were detected by quantitative real time polymerase chain reaction (qRT-PCR). Western blot was employed to determine the protein expression levels of MYO6 and proliferating cell nuclear antigen (PCNA). The effects of hsa_circ_0000231 on cell proliferation, apoptosis, migration, and invasive in CRC were determined by cell counting kit-8 proliferation (CCK-8) and colony formation assays, flow cytometry analysis, wound-healing assay, and transwell invasion assay, respectively. Glucose uptake and lactate production were severally illustrated by glucose assay kit and lactate assay kit. The relationship between miR-502-5p and hsa_circ_0000231 or MYO6 was predicted by circular RNA interactome or targetScan online databases, and identified by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. In vivo tumor formation assay was carried out to determine the effects of hsa_circ_0000231 knockdown on tumor growth in vivo. Results Hsa_circ_0000231 expression was dramatically upregulated while miR-502-5p was obviously downregulated in CRC tissues and cells compared with control groups. Hsa_circ_0000231 knockdown repressed the expression levels of MYO6 and PCNA protein. Functionally, hsa_circ_0000231 knockdown repressed cell glycolysis, proliferation, migration and invasion, and induced cell apoptosis, whereas these effects were decreased by miR-502-5p inhibitor. Mechanistically, hsa_circ_0000231 acted as a sponge of miR-502-5p and miR-502-5p bound to MYO6. Furthermore, hsa_circ_0000231 knockdown decreased tumor volume and weight of CRC in vivo. Conclusion Hsa_circ_0000231 knockdown inhibited CRC progression and glycolysis by downregulating MYO6 expression through sponging miR-502-5p, which might provide a theoretical basis in further studying circ_0000231-directed therapy in CRC.

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CCND1, NOP14 and DNMT3B are involved in miR‐502‐5p–mediated inhibition of cell migration and proliferation in bladder cancer

Cited by 47 publications

References 39 publications

MicroRNA-381 inhibits bladder cancer pathogenesis through directly controlling BMI1 and triggering the Rho/ROCK signaling pathway defect

MicroRNA-381 inhibits bladder cancer pathogenesis through directly controlling BMI1 and triggering the Rho/ROCK signaling pathway defect

Role of microRNA-381 in bladder cancer growth and metastasis with the involvement of BMI1 and the Rho/ROCK axis

Hsa_circ_0000231 knockdown inhibits the glycolysis and progression of colorectal cancer cells by regulating miR-502-5p/MYO6 axis

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