Epigenetic disruption of miR-130a promotes prostate cancer by targeting SEC23B and DEPDC1

Ramalho-Carvalho, João; Martins, João Barbosa; Cekaite, Lina; Sveen, Anita; Torres-Ferreira, Jorge; Graça, Inês; Costa-Pinheiro, Pedro; Eilertsen, Ina A.; Antunes, Luís; Oliveira, Jorge; Lothe, Ragnhild; Henrique, Rui; Jerónimo, Carmen

doi:10.1016/j.canlet.2016.10.028

Cited by 60 publications

(53 citation statements)

References 43 publications

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“…In previous studies, miR-130a-3p was usually reported to act as a tumor suppressor in various type of cancers (21,29,30) or a repressor in adipocyte tissue inhibiting the induction of preadipocytes into mature adipocytes (31). In this study, we firstly confirmed miR-130a-3p inhibited PRL expression, suggesting that miR-130a-3p may be involved in pituitary hormone regulation.…”

Section: Discussionsupporting

confidence: 76%

MiR-130a-3p Inhibits PRL Expression and Is Associated With Heat Stress-Induced PRL Reduction

et al. 2020

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MicroRNAs (MiRNAs) play critical roles in the regulation of pituitary function. MiR-130a-3p has previously been found to be down-regulated in prolactinoma, but its roles in prolactin (PRL) regulation and the underlying mechanisms are still unclear. Heat stress has been shown to induce alteration of endocrine hormones and miRNAs expressions. However, there is limited information regarding the emerging roles of miRNAs in heat stress response. In this study, we transfected miR-130a-3p mimic into the pituitary adenoma cells (GH3 cells) to investigate the function of miR-130a-3p in regulating PRL. Our results showed that miR-130a-3p overexpression significantly decreased the PRL expression at both mRNA and protein levels. Subsequently, estrogen receptor α (ERα) was identified as a direct target of miR-130a-3p by bioinformatics prediction, luciferase reporter assay and western blotting assay. Furthermore, the inhibition of ERα caused by estrogen receptor antagonist significantly reduced the PRL expression. Overexpression of ERα rescued the suppressed expression of PRL caused by miR-130a-3p mimic. Besides, we also studied the effect of heat stress on PRL and miRNAs expressions. Interestingly, we found that heat stress reduced PRL and ERα expressions while it increased miR-130a-3p expression both in vitro and in vivo. Taken together, our results indicate that miR-130a-3p represses ERα by targeting its 3'UTR leading to a decrease in PRL expression, and miR-130a-3p is correlative with heat stress-induced PRL reduction, which provides a novel mechanism that miRNAs are involved in PRL regulation.

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Section: Discussionsupporting

confidence: 76%

MiR-130a-3p Inhibits PRL Expression and Is Associated With Heat Stress-Induced PRL Reduction

et al. 2020

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“…Consistent with these results, Qu et al (13) demonstrated that DEPDC1 knockdown inhibited HCC cell proliferation, colony formation, migration and invasion. In addition, DEPDC1 silencing via siRNA reduced the viability and invasion capability of prostate cancer cell lines (24), while DEPDC1 upregulation promoted prostate cancer cell proliferation and metastases (25). Collectively, the data indicated that DEPDC1 may serve an important oncogenic role in HCC progression.…”

Section: Discussionmentioning

confidence: 83%

DEPDC1 drives hepatocellular carcinoma cell proliferation, invasion and angiogenesis by regulating the CCL20/CCR6 signaling pathway

Guo

Liu

et al. 2019

Oncol Rep

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DEP domain containing 1 (DEPDC1) functions as an oncogene in hepatocellular carcinoma (HCC). However, the underlying mechanism of DEPDC1 remains largely unknown. The present study revealed that DEPDC1 knockdown inhibited HCC cell proliferation, colony formation and invasion in vitro and suppressed the growth of HCC xenografts in vivo. Furthermore, DEPDC1 overexpression promoted HCC cell proliferation, colony formation and invasion. DNA microarray, reverse transcription-quantitative-PCR and western blotting results demonstrated that DEPDC1 knockdown in Huh-7 significantly inhibited the expression of chemokine (C-C motif) ligand 20 (CCL20) and chemokine (C-C motif) receptor 6 (CCR6). In addition, the expression of CCL20 and CCR6 were upregulated in HCC tissues and cell lines, and were positively correlated with DEPDC1 expression. CCL20 or CCR6 knockdown via small interfering RNA reversed the effects of DEPDC1 overexpression in HCC cells. Furthermore, it was revealed that conditioned medium from DEPDC1 upregulated Li-7 and Hep3B cells led to angiogenesis in vitro, whereas CCL20 knockdown in Li-7 and Hep3B cells or CCR6 knockdown in human umbilical vein endothelial cells reversed the angiogenic effect of DEPDC1 overexpression. In conclusion, DEPDC1 facilitated cell proliferation, invasion and angiogenesis via the CCL20/CCR6 pathway in HCC.

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“…**P < 0.01; *** P < 0.001 Moreover, miR-130a, acting as a tumor suppressor miRNA, epigenetically downregulated DEPDC1 expression and changed key molecular and phenotypic features in prostate carcinogenesis. 29 In the present study, we carried out a combination of transcriptomic analyses evaluated by Kaplan-Meier analysis to investigate the correlation between the expression level of oncogenic TF genes with patient prognosis in TCGA HCC tissue samples.…”

Section: Discussionmentioning

confidence: 99%

DEP domain containing 1 predicts prognosis of hepatocellular carcinoma patients and regulates tumor proliferation and metastasis

Cui

Lü

et al. 2018

Cancer Science

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DEP domain containing 1 (DEPDC1) protein is a novel oncoantigen upregulated in multiple types of cancers which present oncogenic activity and high immunogenicity. However, the function and therapeutic potential of DEPDC1 in hepatocellular carcinoma (HCC) remain unclear. In the present study, we showed that DEPDC1 was frequently upregulated in HCC and associated with cancer diagnosis and poor prognosis for HCC patients. Moreover, DEPDC1 promotes HCC cell proliferation in vitro as well as carcinogenesis in vivo. Notably, DEPDC1 overexpression also increases the neoplasm metastasis ability of HCC cells both in vivo and in vitro. Gene set enrichment analysis results showed that DEPDC1 expression is positively correlated with K‐RAS signal pathway, pathways in cancer and WNT/β‐catenin signal pathway, all of which are closely associated with specific cancer‐related gene sets. Our study provides the basis for further investigation of the molecular mechanism by which DEPDC1 promotes the development and metastasis of HCC.

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Epigenetic disruption of miR-130a promotes prostate cancer by targeting SEC23B and DEPDC1

Cited by 60 publications

References 43 publications

MiR-130a-3p Inhibits PRL Expression and Is Associated With Heat Stress-Induced PRL Reduction

MiR-130a-3p Inhibits PRL Expression and Is Associated With Heat Stress-Induced PRL Reduction

DEPDC1 drives hepatocellular carcinoma cell proliferation, invasion and angiogenesis by regulating the CCL20/CCR6 signaling pathway

DEP domain containing 1 predicts prognosis of hepatocellular carcinoma patients and regulates tumor proliferation and metastasis

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