MicroRNA-30a functions as tumor suppressor and inhibits the proliferation and invasion of prostate cancer cells by down-regulation of SIX1

Zhu, Qinghuan; Zhang, Lipeng; Li, Yingjie; Jiang, Lining

doi:10.1007/s13577-017-0170-1

Cited by 23 publications

(22 citation statements)

References 32 publications

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“…Many studies have reported that SIX1 downregulation significantly decreases proliferation in many cancer cell types including prostate cancer, oral squamous cell carcinoma, nonsmall cell lung cancer, and hepatocellular carcinoma. [25][26][27][28] A common target of SIX1 is cyclin D1, which is significantly upregulated after overexpressing SIX1. 13,27,29 However, the effect of SIX1 on GC proliferation remained unknown.…”

Section: Discussionmentioning

confidence: 99%

SIX1 is upregulated in gastric cancer and regulates proliferation and invasion by targeting the ERK pathway and promoting epithelial‐mesenchymal transition

Xie

Peng

Sun

et al. 2018

Cell Biochemistry & Function

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Sine oculis homeobox homologue 1 (SIX1) is a Six class homeobox gene conserved throughout many species. It has been reported to act as an oncogene and is overexpressed in many cancers. However, the function and regulatory mechanism of SIX1 in gastric cancer (GC) remains unclear. In our study, we detected protein levels of SIX1 via immunohistochemistry (IHC) and its proliferation and invasion effects via CCK8 and transwell assays. Additionally, expression of cyclin D1, MMP2, p‐ERK, and EMT‐related proteins was measured by western blotting. We found that SIX1 had significantly higher expression in GC tissues and that it could promote GC cell proliferation and invasion. Also, overexpression of SIX1 increased the expression of cyclin D1, MMP2, p‐ERK, and EMT‐related proteins, which could all be inhibited by knocking down SIX1. In conclusion, SIX1 is upregulated in GC tissues. It can promote GC cell proliferation by targeting cyclin D1, invasion via ERK signalling, and EMT pathways by targeting MMP2 and E‐cadherin. Significance of the study Our study showed that SIX1 was upregulated in GC tissues, and promoted GC cell proliferation by targeting cyclin D1, invasion via ERK signalling, and EMT pathways by targeting MMP2 and E‐cadherin. These results suggested the potential regulatory mechanism of SIX1 in proliferation and invasion of gastric cancer.

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Section: Discussionmentioning

confidence: 99%

SIX1 is upregulated in gastric cancer and regulates proliferation and invasion by targeting the ERK pathway and promoting epithelial‐mesenchymal transition

Xie

Peng

Sun

et al. 2018

Cell Biochemistry & Function

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“…miR‐30a has been shown to play an inhibitory role in many cancers, such as cancers of the colon, breast, and lung 38‐40 . miR‐30a has also been previously reported to function as a tumor suppressor in PCa 12,13,15,16,41 . miR‐30a inhibits proliferation, 15,16 invasion and epithelial‐mesenchymal transition of PCa cells 12,41 .…”

Section: Discussionmentioning

confidence: 97%

“…Previously, we and others have shown that the aberrant expression of miR‐30a is associated with epithelial‐mesenchymal transition, radiosensitivity, proliferation, and invasion in PCa 12‐16 . To the best of our knowledge, the role of miR‐30a in CRPC has not been fully elucidated.…”

Section: Introductionmentioning

confidence: 93%

miR‐30a inhibits androgen‐independent growth of prostate cancer via targeting MYBL2, FOXD1, and SOX4

et al. 2020

The Prostate

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Background: Castrate-resistant prostate cancer (CRPC) is an aggressive and lethal disease. The pathogenesis of CRPC is not fully understood and novel therapeutic targets need to be identified to improve the patients' prognosis. has been demonstrated to be a tumor suppressor in many types of solid malignancies. However, its role in androgen-independent (AI) growth of prostate cancer (PCa) received limited attention as yet. Methods:The clinical association of miR-30a and its potential targets with AI growth was characterized by bioinformatics analyses. Regulation of cell proliferation and colony formation rates by miR-30a were tested using PCa cell models. Xenograft models were used to measure the regulation of prostate tumor growth by miR-30a.The real-time quantitative polymerase chain reaction was used to validate whether miR-30a and its targets regulate cell cycle control genes and androgen receptor (AR)-dependent transcription. Bioinformatics tools, Western blot, and luciferase reporter assays were utilized to identify miR-30a targets. Results: Bioinformatic analysis showed that low expression of miR-30a is associated with castration resistance of PCa patients and poor outcomes. Transfection of miR-30a mimics inhibited the AI growth of PCa cells in vitro and in vivo. Upregulation of miR-30a in 22RV1 cells altered the expression of cell cycle control genes and AR-mediated transcription, while downregulation of miR-30a in LNCaP cells had the opposite effects to AR-mediated transcription. MYBL2, FOXD1, and SOX4 were identified as miR-30a targets. Downregulation of MYBL2, FOXD1, and SOX4 affected the expression of cell cycle control genes and AR-mediated transcription and suppressed the AI growth of 22RV1 cells. Conclusions: Our results suggest that miR-30a inhibits AI growth of PCa by targeting MYBL2, FOXD1, and SOX4. They provide novel insights into developing new treatment strategies for CRPC. K E Y W O R D S castration-resistant prostate cancer, FOXD1, miR-30a, MYBL2, SOX4

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“…Additionally, a previous study shows that miR‐204‐5p negatively regulates SIX1 expression and suppresses cell proliferation in HCC . In other diseases, miR‐30a, miR‐362, and miR‐185 have also been described to regulate the expression of SIX1 . Of these, miR‐362 is significantly upregulated in HCC tissues, suggesting that it might not target SIX1 in HCC.…”

Section: Discussionmentioning

confidence: 99%

“…63 In other diseases, miR-30a, miR-362, and miR-185 have also been described to regulate the expression of SIX1. [64][65][66] Of these, miR-362 is significantly upregulated in HCC tissues, 67 suggesting that it might not target SIX1 in HCC. In addition, miR-30a and miR-185 are decreased and are known to suppress HCC progression.…”

Section: Discussionmentioning

confidence: 99%

LncRNA CRNDE promotes hepatocellular carcinoma progression by upregulating SIX1 through modulating miR‐337‐3p

Tang

Zhao

Peng

et al. 2019

J of Cellular Biochemistry

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Background Long noncoding RNA (lncRNA) is emerging as a vital regulator in various cancers. Recently, it was found that lncRNA colorectal neoplasia differentially expressed (CRNDE) plays an oncogenic role, promoting cell proliferation and migration in hepatocellular carcinoma (HCC). However, the underlying regulatory mechanism of lncRNA CRNDE remains unclear. Methods The expression levels of lncRNA CRNDE and miR‐337‐3p were analyzed by real‐time polymerase chain reaction, and sineoculis homeobox homolog 1 (SIX1) expression was determined by Western blot analysis. RNA pull‐down, luciferase and Western blot analysis assays were used to examine the target relationship between lncRNA CRNDE and miR‐337‐3p as well as between miR‐337‐3p and SIX1. The functional effects of lncRNA CRNDE and miR‐337‐3p were examined in vitro by using cell viability, colony formation, wound scratch, transwell assays, and in vivo in a xenograft tumor mouse model. Results LncRNA CRNDE was overexpressed in tumor tissues of patients with HCC. LncRNA CRNDE downregulation significantly suppressed cell proliferation and migration. Mechanistic investigations demonstrated that lncRNA CRNDE interacted with miR‐337‐3p and decreased its expression, thereby increasing the protein expression of miR‐337‐3p's target, SIX1. In addition, in vivo experiments using a xenograft tumor mouse model revealed that lncRNA CRNDE served as an oncogene, partly through sponging miR‐337‐3p and upregulating SIX1 in HCC. Conclusions In this study, we report a newly identified regulatory mechanism lncRNA CRNDE/miR‐337‐3p/SIX1 axis, suggesting a promising therapeutic target in HCC.

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MicroRNA-30a functions as tumor suppressor and inhibits the proliferation and invasion of prostate cancer cells by down-regulation of SIX1

Cited by 23 publications

References 32 publications

SIX1 is upregulated in gastric cancer and regulates proliferation and invasion by targeting the ERK pathway and promoting epithelial‐mesenchymal transition

SIX1 is upregulated in gastric cancer and regulates proliferation and invasion by targeting the ERK pathway and promoting epithelial‐mesenchymal transition

miR‐30a inhibits androgen‐independent growth of prostate cancer via targeting MYBL2, FOXD1, and SOX4

LncRNA CRNDE promotes hepatocellular carcinoma progression by upregulating SIX1 through modulating miR‐337‐3p

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