miR‐152 controls migration and invasive potential by targeting TGFα in prostate cancer cell lines

Zhu, Chen; Li, Jie; Ding, Qi; Cheng, Gong; Zhou, Hai; Liu, Tao; Cai, Hongzhou; Li, Pu; Cao, Qiang; Ju, Xingrong; Meng, Xia; Qin, Chao; Liu, Hua; Shao, Pengfei; Chen, Yin

doi:10.1002/pros.22656

Cited by 77 publications

(75 citation statements)

References 18 publications

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“…We also proved that Wnt-1 was another target of miR-152 in HCC, which was consistent with Huang et al (2014). The cholecystokinin B receptor (CCKBR) (Chen et al, 2010c), colony stimulating factor-1 (CSF-1) (Woo et al, 2012) and transforming growth factor-alpha (TGFα) (Zhu et al, 2013) were also found as putative targets of miR-152 in different cancers (Chen et al, 2010c). However, none of these genes were influenced by miR-152 mimic in HepG2 cells in the current study (data not shown).…”

Section: Discussionsupporting

confidence: 67%

Effects of miR-152 on Cell Growth Inhibition, Motility Suppression and Apoptosis Induction in Hepatocellular Carcinoma Cells

Dang¹,

Zeng²,

He³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Background: miR-152 is involved in the genesis and development of several malignancies. However, its role in HCC has not been fully clarified. The aim of this study was to investigate the clinicopathological significance of miR-152 and its effect on the malignant phenotype of HCC cells. Methods: miR-152 expression was detected using real-time quantitative RT-PCR in 89 pairs of HCC formalin-fixed paraffin-embedded and their adjacent tissues. Functionally, in vitro effects and mechanisms of action of miR-152 on proliferation, viability, caspase activity, apoptosis and motility were explored in HepG2, HepB3 and SNU449 cells, as assessed by spectrophotometry, fluorimetry, fluorescence microscopy, wound-healing and Western blotting, respectively. Results: miR-152 expression in HCC was downregulated remarkably compared to that in adjacent hepatic tissues. miR-152 levels in groups of advanced clinical stage, larger tumor size and positive HBV infection, were significantly lower than in other groups. A miR-152 mimic could suppress cell growth, inhibit cell motility and increase caspase activity and apoptosis in HCC cell lines. Furthermore, Western blotting showed that the miR-152 mimic downregulated Wnt-1, DNMT1, ERK1/2, AKT and TNFRS6B signaling. Intriguingly, inverse correlation of TNFRF6B and miR-152 expression was found in HCC and bioinformatics confirmed that TNFRF6B might be a target of miR-152. Conclusions: Underexpression of miR-152 plays a vital role in hepatocarcinogenesis and lack of miR-152 is related to the progression of HCC through deregulation of cell proliferation, motility and apoptosis. miR-152 may act as a tumor suppressor miRNA by also targeting TNFRSF6B and is therefore a potential candidate biomarker for HCC diagnosis, prognosis and molecular therapy.

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Section: Discussionsupporting

confidence: 67%

Effects of miR-152 on Cell Growth Inhibition, Motility Suppression and Apoptosis Induction in Hepatocellular Carcinoma Cells

Dang¹,

Zeng²,

He³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…The aberrant expression of miRNAs is closely related to proliferation, cell cycle, apoptosis, differentiation, migration, metabolism, and prognosis of various cancers, including PCa (Xu et al, 2012;Zhu et al, 2013;Liu et al, 2014). Until now, more than 50 miRNAs have been found to be involved in PCa, but only few studies have successfully identified miRNA targets that are specifically modulated in PCa (Wu et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

microRNA-372 Suppresses Migration and Invasion by Targeting p65 in Human Prostate Cancer Cells

Kong

Qian²,

Duan

et al. 2016

DNA and Cell Biology

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Prostate cancer (PCa) is one of the most prevalent malignant tumors. microRNAs (miRNAs) play an important role in cancer initiation, progression, and metastasis, and their roles in PCa are becoming more apparent. In this study, we found that microRNA-372 (miR-372) is downregulated in human PCa and inhibits the proliferation activity, migration, and invasion of DU145 cells. Subsequently, p65 is confirmed as a target of miR-372, and knockdown of p65 expression similarly resulted in decreased proliferation activity, migration, and invasion. CDK8, MMP-9, and prostate-specific antigen were involved in both these processes. Taken together, our results show evidence that miR-372 may function as a tumor suppressor gene by regulating p65 in PCa and may provide a strategy for blocking PCa metastasis.

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“…The authors of one report have suggested that miR-152 acts as a tumor suppressor in prostate cancer by targeting the 3'UTR of TGF-α (Zhu et al, 2013). Other researchers reported epigenetic silencing by DNA hypermethylation of miR-152 in endometrial cancer, and restoration of miR-152 expression in endometrial cancer cell lines resulted in inhibition of tumor cell growth, both in vitro and in vivo (Tsuruta et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

A microRNA-152 that targets the phosphatase and tensin homolog to inhibit low oxygen induced-apoptosis in human brain microvascular endothelial cells

Cao

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Brain damage caused by perinatal asphyxia is dangerous for neonatal infants, but the mechanism by which it occurs remains elusive. In this study, microRNA-152 (miR-152) expression was induced by low oxygen levels in rat models of hypoxia brain damage, as well as in human brain microvascular endothelial cells (HBMECs) cultured in vitro. Analysis of the sequence of miR-152 revealed that the phosphatase and tensin homolog gene (PTEN) is probably the target of miR-152 both in humans and rats. When HBMECs were transfected with miR-152 mimics, PTEN expression was inhibited at both the mRNA and protein levels. Moreover, transfection with the miR-152 mimic also inhibited apoptosis induced by hypoxia. Furthermore, expression of the pro-apoptotic gene Bax was downregulated while the anti-apoptotic gene Bcl2 was upregulated after miR-152 mimic transfection. Taken together, these results indicate that miR-152 induced by hypoxia suppresses cell apoptosis and acts as a protective factor during hypoxia by repressing PTEN.

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miR‐152 controls migration and invasive potential by targeting TGFα in prostate cancer cell lines

Abstract: Our findings suggest that miR-152 can act as a tumor suppressor that targets TGFα. miR-152 is a promising molecular target that inhibits PCa cell migration and invasion.

Cited by 77 publications

References 18 publications

Effects of miR-152 on Cell Growth Inhibition, Motility Suppression and Apoptosis Induction in Hepatocellular Carcinoma Cells

Effects of miR-152 on Cell Growth Inhibition, Motility Suppression and Apoptosis Induction in Hepatocellular Carcinoma Cells

microRNA-372 Suppresses Migration and Invasion by Targeting p65 in Human Prostate Cancer Cells

A microRNA-152 that targets the phosphatase and tensin homolog to inhibit low oxygen induced-apoptosis in human brain microvascular endothelial cells

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