MicroRNA-542-3p suppresses cellular proliferation of bladder cancer cells through post-transcriptionally regulating survivin

Zhang, Jiajun; Wang, Sheng; Han, Feng; Li, Jian; Lan, Yu; Zhou, Ping; Chen, Zhijun; Xue, Sheng; Dai, Changyuan; Li, Qingwen

doi:10.1016/j.gene.2015.12.048

Cited by 36 publications

(23 citation statements)

References 16 publications

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“…Investigation of the corresponding region in BIRC5 identified no Eomes interactions (data not shown), consistent with prior work that detected Eomes on BIRC2 , BIRC6 , and BIRC7 , but not on BIRC5 [6]. Post-transcriptional regulation of BMF and BIRC5 also might be an important mechanism, via the actions of one or more microRNAs [24–27], which also serve to regulate Eomes [28,29]. Further studies are warranted on the reciprocal regulation of BMF and BIRC5 in response to changes in Eomes expression.…”

Section: Discussionsupporting

confidence: 87%

Reciprocal regulation of BMF and BIRC5 (Survivin) linked to Eomes overexpression in colorectal cancer

et al. 2016

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Eomesodermin (Eomes) is a T-box transcription factor that has been implicated in the etiology of colorectal cancer and other human malignancies. We screened a panel of human primary colon cancers and patient-matched controls (n = 30) and detected Eomes overexpression at the mRNA and protein level. Similar results were obtained in a panel of rat colon tumors and adjacent normal-looking colonic mucosa (n = 24). In human colon cancer cells, forced overexpression of Eomes enhanced cell viability and protected against staurosporine-induced apoptosis. On the other hand, knocking down Eomes resulted in reduced cell viability, G2/M cell cycle arrest, and apoptosis induction. The apoptotic mechanism centered on the reciprocal downregulation of anti-apoptotic BIRC5 (Survivin) and upregulation of proapoptotic Bcl-2 modifying factor (BMF). In patients with colorectal cancer, high EOMES expression (n = 95) was associated with poor overall survival compared with individuals exhibiting low EOMES levels (n = 80). We conclude from the current investigation, and prior literature, that Eomes has a divergent role in cancer development, with evidence for tumor suppressor and oncogenic functions, depending on stage and tissue context. Further studies are warranted on the apoptotic mechanisms linked to the reciprocal regulation of BMF and BIRC5 in human colorectal cancers characterized by Eomes overexpression.

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Section: Discussionsupporting

confidence: 87%

Reciprocal regulation of BMF and BIRC5 (Survivin) linked to Eomes overexpression in colorectal cancer

et al. 2016

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“…These results suggested that SETDB1 were indeed up-regulated in CRC as well as in other solid tumors [22,24]. On the other hand, survivin is an oncogene that regulates the apoptosis, proliferation, and invasion of many cancers [25][26][27]. Knockdown of survivin by using siRNA could dramatically suppress the proliferation and invasion of bladder cancer cells [8].…”

Section: Discussionmentioning

confidence: 93%

LncRNA FENDRR represses proliferation, migration and invasion through suppression of survivin in cholangiocarcinoma cells

Qin

Zhou

et al. 2019

Cell Cycle

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This study was to investigate the biological function and underlying mechanisms of FENDRR in cholangiocarcinoma (CCA) cell proliferation, migration and invasion. FENDRR and survivin expression in CCA tissues or cell lines were measured by qRT-PCR. In QBC939 and HuCCTl cells, cell proliferation was detected by CCK-8, cell migration and invasion were using transwell assay. RNA pull-down and RIP assay were performed to determine whether FENDRR can combine with SETDB1 in CCA cell. The effect of SETDB1 on survivin and H3K9me1 expression in CCA cells were determined by western blotting. ChIP analysis was performed to analyze the combination of SETDB1 with survivin promoter in CCA cell. The effect of SETDB1 knockdown on survivin and H3K9me1 expression in CCA cells after transfection with FENDRR were determined by western blotting. The results showed that lncRNA FENDRR was downregulated in CCA tissues and cells, and was negatively correlated with survivin expression. Further investigation demonstrated that FENDRR represses CCA cell proliferation, migration and invasion through regulating survivin expression. FENDRR associated with SETDB1 and H3K9 to epigenetically silence survivin and then regulated cell proliferation, migration and invasion. These findings indicate an important role for FENDRR-survivin axis in CCA cell proliferation, migration and invasion, and reveal a novel epigenetic mechanism for survivin silencing. Our data indicated that FENDRR silences survivin via SETDB1-mediated H3K9 methylation, thereby represses CCA cell proliferation, migration and invasion. ARTICLE HISTORY

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“…[5][6][7] The overall 5-year survival rate is approximately 75%, and a significant influence factor is the time of diagnosis. 8 A popular current research topic is targeted therapy. Targeted therapy acts on the genetic pathways responsible for BC, 4 which is regarded as the nextgeneration therapy for the disease with the help of genomic and proteomic techniques.…”

Section: Introductionmentioning

confidence: 99%

MiR-1-3p inhibits the proliferation and invasion of bladder cancer cells by suppressing CCL2 expression

et al. 2017

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We attempted to analyze the effects of miR-1-3p and CCL2 on the proliferation, migration, and invasion of bladder cancer cells. A total of 18 pairs of bladder cancer tissues with corresponding adjacent tissues and the 6 cases of normal tissues were collected. The expressions of miR-1-3p and CCL2 in the cancer tissues were evaluated using quantitative real-time polymerase chain reaction and western blot. The relationship between miR-1-3p and CCL2 was assessed using luciferase reporter assay. The UM-UC-3 bladder cancer cells were transfected with CCL2 small interfering RNA and miR-1-3p mimics. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, colony formation assay, wound healing assay, Transwell assay, and the flow cytometry test were used to detect the proliferation, migration, invasion, and apoptosis of bladder cancer cells. Bladder cancer tissues had lower levels of miR-1-3p but higher levels of CCL2 than normal tissues (p < 0.05). The transfection of miR-1-3p mimics and CCL2 small interfering RNA remarkably suppressed cell proliferation and invasion and promoted apoptosis of cells (p < 0.05). Results of the luciferase reporter gene assay demonstrated that miR-1-3p targeted CCL2. MiR-1-3p suppresses the proliferation and invasion of urinary bladder cancer cells by targeting CCL2.

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MicroRNA-542-3p suppresses cellular proliferation of bladder cancer cells through post-transcriptionally regulating survivin

Cited by 36 publications

References 16 publications

Reciprocal regulation of BMF and BIRC5 (Survivin) linked to Eomes overexpression in colorectal cancer

Reciprocal regulation of BMF and BIRC5 (Survivin) linked to Eomes overexpression in colorectal cancer

LncRNA FENDRR represses proliferation, migration and invasion through suppression of survivin in cholangiocarcinoma cells

MiR-1-3p inhibits the proliferation and invasion of bladder cancer cells by suppressing CCL2 expression

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