Identification of Novel AR-Targeted MicroRNAs Mediating Androgen Signalling through Critical Pathways to Regulate Cell Viability in Prostate Cancer

Mo, Wenjuan; Zhang, Jiyuan; Li, Xia; Meng, Delong; Gao, Yun; Yang, Shu; Zhou, Chang; Guo, Fuyu; Huang, Yan; Amente, Stefano; Avvedimento, Enrico V.; Xie, Yun; Li, Yao

doi:10.1371/journal.pone.0056592

Cited by 102 publications

(100 citation statements)

References 47 publications

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“…In this study, androgens stimulating miR-19a, and miR-19a directly repressing ABCA1 mRNA expression, may represent a possible mechanism underlying androgen-mediated repression of ABCA1, promoting PCa cell proliferation (55). The activation of ABCA1 was also shown to inhibit the proliferation of androgen-dependent prostate cancer cells, and androgen treatment in LNCaP cells significantly inhibited the expression of ABCA1 mRNA (56).…”

Section: Abca1 and Multidrug Resistance (Mdr)mentioning

confidence: 66%

ATP‑binding cassette transporter A1: A promising therapy target for prostate cancer (Review)

Xiong

Huang

et al. 2017

mol clin onc

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Abstract. ATP-binding cassette transporter A1 (ABCA1) has been found to mediate the transfer of cellular cholesterol across the plasma membrane to apolipoprotein A-I (apoA-I), and is essential for the synthesis of high-density lipoprotein.Mutations of the ABCA1 gene may induce Tangier disease and familial hypoalphalipoproteinemia; they may also lead to loss of cellular cholesterol homeostasis in prostate cancer, and increased intracellular cholesterol levels are frequently found in prostate cancer cells. Recent studies have demonstrated that ABCA1 may exert anticancer effects through cellular cholesterol efflux, which has been attracting increasing attention in association with prostate cancer. The aim of the present review was to focus on the current views on prostate cancer progression and the various functions of ABCA1, in order to provide new therapeutic targets for prostate cancer.

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Section: Abca1 and Multidrug Resistance (Mdr)mentioning

confidence: 66%

ATP‑binding cassette transporter A1: A promising therapy target for prostate cancer (Review)

Xiong

Huang

et al. 2017

mol clin onc

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“…The expressed alleles of the myomiRs can be assessed accurately by employing pri or premiR RTPCR assays. For example, only cistron miR12/133a1 is found expressed in AML, presumably due to specific activation of that cistron [120] and amongst the myomiRs only premiR133b is elevated in cervical cancer [121] , in bladder cancer [122] , and in progressive prostate cancer [123] . We suggest that initial microarray profiling be confirmed by pri-or premiRNA assay of each miR isomer independently.…”

Section: Cancer and Downregulated Myomirsmentioning

confidence: 99%

Roles of the canonical myomiRs miR-1, -133 and -206 in cell development and disease

Mitchelson¹

2015

WJBC

136

132

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MicroRNAs are small non-coding RNAs that participate in different biological processes, providing subtle combinational regulation of cellular pathways, often by regulating components of signalling pathways. Aberrant expression of miRNAs is an important factor in the development and progression of disease. The canonical myomiRs (miR-1, -133 and -206) are central to the development and health of mammalian skeletal and cardiac muscles, but new findings show they have regulatory roles in the development of other mammalian non-muscle tissues, including nerve, brain structures, adipose and some specialised immunological cells. Moreover, the deregulation of myomiR expression is associated with a variety of different cancers, where typically they have tumor suppressor functions, although examples of an oncogenic role illustrate their diverse function in different cell environments. This review examines the involvement of the related myomiRs at the crossroads between cell development/ tissue regeneration/tissue inflammation responses, and cancer development. Core tip: The roles of the canonical muscle-associated microRNAs are reviewed, including microRNA families miR-1 and miR-133, and single miR-206, which are collectively known as the "myomiRs". The myomiRs act at the crossroads of the molecular regulation of muscle cells, linking between pathways for cell differentiation, development and maintenance, but also potentiate aberrant cell growth in numerous non-muscle cancers. Typically myomiRs are downregulated in cancers, but some myomiRs are upregulated in a few cancers, yet each dysregulation event advances tumor progression. The review examines normal and disease-linked molecular changes associated with the myomiRs, and collates the extensive literature into accessible tables. REVIEW

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“…There is a significant difference in the expression level of miRs in cancerous tissue and normal tissue (4). Based on their diversity and wide distribution throughout the genome, miRs may serve as an important tumor diagnostic method (5).…”

Section: Introductionmentioning

confidence: 99%

Role of microRNA-4458 in patients with non-small-cell lung cancer

et al. 2016

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Abstract. Incidence and progression of non-small-cell lung cancer (NSCLC) is a multi-factor, multi-step process. The present study investigated the association between the expression level of microRNA (miR)-4458 in NSCLC and paracarcinoma liver tissues and survival rates, and studied the biological functions of miR-4458 at the cellular and protein level. NSCLC and paracarcinoma tissues were sequenced using a miR expression chip. The association between miR-4458 expression and tumor-node-metastasis staging, total survival rate and relapse-free survival rate was analyzed. miR-4458 was subjected to target gene prediction. The target protein of cyclin D1 (CCND1) was verified with western blot analysis, immunohistochemistry and a luciferase reporter assay. The relative level of miR-4458 in paracarcinoma tissues of 9 NSCLC patients decreased from 2.38 to 0.65 (P<0.001). Total five-year survival rates of the high-expression miR-4458 group (29.21%) significantly exceeded that of the low-expression group (14.37%) (P=0.025). The viability of human lung carcinoma A549 and H460 cells transfected with miR-4458 decreased significantly compared with cells transfected with a normal control (blank control plasmid) within 72 h (P<0.001). The percentage of A549 and H460 cells transfected with a miR-4458 mimic at the cell cycle stage G0/G1 was 69.94±8.05 and 68.15±7.75%, respectively. The percentages increased significantly compared with the control group (46.06±6.93 for A549 cells; 45.22±7.24 for H640 cells; P<0.001). CCND1 mRNA was downregulated significantly in H460 cells 72 h subsequent to the addition of miR-4458 mimics (P<0.001). The activity of mutant-CCND1 altered slightly, while the fluorescence intensity of the wild-type-CCND1 group decreased significantly following the addition of miR-4458 mimics. In conclusion, miR-4458 was expressed at low levels in lung cancer tissues, and it arrested cells in vitro at stage G0/G1 and inhibited cell proliferation. Therefore, miR-4458 may participate in the onset of lung cancer as a suppressor gene by inhibiting CCND1.

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Identification of Novel AR-Targeted MicroRNAs Mediating Androgen Signalling through Critical Pathways to Regulate Cell Viability in Prostate Cancer

Cited by 102 publications

References 47 publications

ATP‑binding cassette transporter A1: A promising therapy target for prostate cancer (Review)

ATP‑binding cassette transporter A1: A promising therapy target for prostate cancer (Review)

Roles of the canonical myomiRs miR-1, -133 and -206 in cell development and disease

Role of microRNA-4458 in patients with non-small-cell lung cancer

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