MiR-4638-5p inhibits castration resistance of prostate cancer through repressing Kidins220 expression and PI3K/AKT pathway activity

Yang, Wancai; Ninghan, F.N.H.

doi:10.1016/s1569-9056(18)33035-5

Cited by 9 publications

(17 citation statements)

References 62 publications

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“…Meta‐analysis of 10 PCa miRNA microarray studies, including benign prostate and PCa tissue samples, uncovered 101 miRNAs to be distinctly and differentially expressed ( P < .01) (Table S4 and Figure S1). Next, after converging the differential miRNAs between ADPC and CRPC in the two datasets (GSE80400 and Wang et al, 32 fold change ≥ 2), we found six candidate miRNAs (Figure 1A). Among these six miRNAs, the downregulation of miR‐30a was most significantly associated with poor BCR‐free survival (Figures 1B and S2).…”

Section: Resultsmentioning

confidence: 89%

“…Among these six miRNAs, the downregulation of miR‐30a was most significantly associated with poor BCR‐free survival (Figures 1B and S2). The expression of miR‐30a was decreased in CRPC tissues (Wang et al, 32 Figure 1C). miR‐30a had lower expression in three AI cell lines, PC3, 22RV1, and DU145 than in androgen‐dependent cell lines, LNCaP (Figure 1D).…”

Section: Resultsmentioning

confidence: 90%

“…miR‐30a was downregulated in CRPC and was associated with poor prognosis. A, Venn diagram showing differential miRNAs between ADPC and CRPC in two datasets (GSE80400, Wang et al 32 ) and downregulation miRNAs (Meta_down_ miRNA) by using Meta‐analysis of 10 PCa miRNA microarray studies (supplied in Table S4). B, Kaplan‐Meier survival analysis of miR‐30a expression and biochemical recurrence‐free survival in TCGA (n = 410).…”

Section: Resultsmentioning

confidence: 99%

“…The median value set as cutoff defining miR‐30a high/low expression. C, The expression of miR‐30a in ADPC and CRPC samples (Wang et al 32 ). D, Real‐time qPCR analyses of miR‐30a expression in PCa cell lines.…”

Section: Resultsmentioning

confidence: 99%

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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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Section: Resultsmentioning

confidence: 89%

Section: Resultsmentioning

confidence: 90%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

See 2 more Smart Citations

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

et al. 2020

The Prostate

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“…Different to HIF‐1α, HIF‐2α is active under mild or physiological hypoxia (<5% O 2 ), and active even after 48–72 hrs . Some important cellular activities are regulated by HIF‐2α, such as proliferation, invasion, differentiation and metabolism . Despite that the effect of hypoxia in glycolysis has been verified , the effect of HIF‐2α on non‐canonical pathway of glutamine is still unknown in PDAC.…”

Section: Introductionmentioning

confidence: 99%

HIF‐2α regulates non‐canonical glutamine metabolism via activation of PI3K/mTORC2 pathway in human pancreatic ductal adenocarcinoma

Chen

Zhao

et al. 2017

J Cellular Molecular Medi

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Hypoxia‐inducible factor‐2α (HIF‐2α) plays an important role in increasing cancer progression and distant metastasis in a variety of tumour types. We aimed to investigate its biological function and clinical significance in human pancreatic ductal adenocarcinoma (PDAC). A total of 283 paired PDAC tissues and adjacent normal tissues were collected from patients who underwent surgery or biopsy at Sun Yat‐sen Memorial Hospital between February 2004 and October 2016. In this study, we noted that HIF‐2α expression was significantly up‐regulated in PDAC, positively associated with disease stage, lymph‐node metastasis and patient survival, and identified as an independent prognostic factor of PDAC patients. We demonstrated that HIF‐2α silencing could reduce proliferation, migration and invasion of PDAC cells in vitro. The similar effect on growth was demonstrated in vivo. Furthermore, we noted that knock‐down of HIF‐2α significantly decreased the expression of glutamate oxaloacetate transaminase 1 (GOT1). Importantly, we confirmed that the PI3K/mTORC2 pathway promoted GOT1 expression by targeting HIF‐2α. Our study validated HIF‐2α was an important factor in PDAC progression and poor prognosis and may promote non‐canonical glutamine metabolism via activation of PI3K/mTORC2 pathway. Targeting HIF‐2α represents a novel prognostic biomarker and therapeutic target for patients with PDAC.

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Functions of the multi‐interacting protein KIDINS220/ARMS in cancer and other pathologies

Raza

Allegrini

Dumontet

et al. 2017

Genes Chromosomes & Cancer

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Development of an organ and subsequently the whole system from an embryo is a highly integrated process. Although there is evidence that different systems are interconnected during developmental stages, the molecular understanding of this relationship is either not known or only to a limited extent. Nervous system development, amongst all, is maybe the most crucial and complex process. It relies on the correct distribution of specific neuronal growth factors and hormones to the specific receptors. Among the plethora of proteins that are involved in downstream signalling of neuronal growth factors, we find the kinase-D interacting substrate of 220 kDa (KIDINS220), also known as ankyrin-rich repeat membrane spanning (ARMS) protein. KIDINS220 has been shown to play a substantial role in the nervous system and vascular system development as well as in neuronal survival and differentiation. It serves as a downstream regulator for many important neuronal and vascular growth factors such as vascular endothelial growth factor (VEGF), the neurotrophin family, glutamate receptors and ephrin receptors. Moreover, activation and differentiation of B- and T-cells, as well as tumour cell proliferation has also shown to be related to KIDINS220. This review comprehensively summarises the existing research data on this protein, with a particular interest in its role in cancer and in other pathologies.

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MiR-4638-5p inhibits castration resistance of prostate cancer through repressing Kidins220 expression and PI3K/AKT pathway activity

Cited by 9 publications

References 62 publications

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

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

HIF‐2α regulates non‐canonical glutamine metabolism via activation of PI3K/mTORC2 pathway in human pancreatic ductal adenocarcinoma

Functions of the multi‐interacting protein KIDINS220/ARMS in cancer and other pathologies

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