MiR-221 promotes the development of androgen independence in prostate cancer cells via downregulation of HECTD2 and RAB1A

Sun, Tong; Wang, X; He, Housheng Hansen; Sweeney, Christopher J.; Liu, S X; Brown, Myles; Balk, Steven P.; Lee, G-Sm; Kantoff, Philip W.

doi:10.1038/onc.2013.230

Cited by 131 publications

(114 citation statements)

References 49 publications

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“…Yang et al suggested that SIRT1 plays a suppressive role against the tumor promoting action of miR-221 and miR-222 (37). In addition, ADAM17, ARHI and HECTD2 were identified as the target genes of miR-221 and miR-222 (22,38,39). These findings suggest that miR-221 and miR-222 are a therapeutic target.…”

Section: Discussionmentioning

confidence: 97%

miR-222 regulates sorafenib resistance and enhance tumorigenicity in hepatocellular carcinoma

Liu

Zhang

et al. 2014

International Journal of Oncology

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Abstract. The miR-222 cluster has been demonstrated to function as oncomiR in human hepatocellular carcinoma (HCC). miR-222 confers chemotherapy drug resistance in various cancers, including HCC. However, the effects and mechanisms by which miR-222 regulates liver tumorigenicity and confers sorafenib (SOR) resistance remain unclear. Here we first investigated the miR-222 effect on proliferation, cell cycle, apoptosis, migration and invasion of HCC. Our results demonstrated that miRNA inhibitors specially targeting miR-222 significantly suppressed cellular proliferation, migration, invasion and G1/S transition of the cell cycle, and induced cell apoptosis in HepG2 cells. In addition, we investigated whether miR-222 confers SOR resistance in HepG2 cells to explore it roles in acquisition of drug resistance. The results showed that miR-222 inhibitors induced sensitivity to the antitumor effect of sorafenib in human HepG2 cells. Importantly, our study also showed that miR-222 could regulate the expression of phosphorylation PI3K and AKT, which might contribute to miR-222 conferred SOR resistance in HepG2 cells. In conclusion, this study demonstrates that miR-222 can promote cell proliferation, migration and invasion, and decrease cell apoptosis, as well as enhance the resistance of HCC cells to sorafenib miR-222 through activating the PI3K/AKT signaling pathway.

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Section: Discussionmentioning

confidence: 97%

miR-222 regulates sorafenib resistance and enhance tumorigenicity in hepatocellular carcinoma

Liu

Zhang

et al. 2014

International Journal of Oncology

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“…Aberrant expression of miRs has been well described in human GC (Pan et al, 2013). Specifically, miR-221 has been confirmed to be upregulated and may act as an oncogene in many types of human malignancies (Gimenes-Teixeira et al, 2013;Sarkar et al, 2013;Ergun et al, 2014;Sun et al, 2014;Ye et al, 2014a). Liu et al (2012) reported that upregulation of miR-221 in GC correlated with aggressive clinicopathological features and shorter overall survival.…”

Section: Introductionmentioning

confidence: 99%

Propofol suppresses proliferation and invasion of gastric cancer cells via downregulation of microRNA-221 expression

Zt¹,

Hy²,

Fang³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Propofol is one of the extensively and commonly used intravenous anesthetic agents. The current study aimed to evaluate the effects of propofol on the behavior of human gastric cancer cells and the molecular mechanisms of this activity. The effects of propofol on SGC7901 and AGS cell proliferation, apoptosis, and invasion were detected by MTT assay, flow cytometric analysis, and matrigel invasion assay. Real-time polymerase chain reaction (PCR) was used to assess microRNA (miR)-221 expression. miR-221 mimics were transfected into SGC7901 and AGS cells to assess the role of miR-221 in propofol-induced anti-tumor activity. Propofol significantly inhibited cell proliferation and invasion and promoted apoptosis of SGC7901 and AGS cells. Propofol also efficiently reduced miR-221 expression. Moreover, transfection of miR-221 mimics reversed the effects of propofol on the biological behavior of gastric cancer cells. Propofol can effectively inhibit proliferation and invasion and induce apoptosis of gastric cancer cells through, at least partly, downregulation of miR-221 expression.

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“…Several miRNAs (miR-21, miR-31, miR-34 and miR-124) can regulate the androgen receptor expression, and simultaneously, AR can regulate the expression of several miRNAs (miR-21, miR-27a, miR-34, miR-125b, miR-221 and let-7) [65]. Goto et al [66] recently demonstrated that miR-221 and 222 were significantly downregulated in CRPC specimens, even when this cluster was previously described to be upregulated ( Figure 3) [67,68]. This fact shows the dynamic status of miRNAs in the development of PCa, regulating the same miRNA different targets depending on the point of the cancer progression.…”

Section: Role Of Mirnas In Prostate Cancermentioning

confidence: 92%

miRNAs as novel biomarkers in the management of prostate cancer

Filella

Foj

2017

Clinical Chemistry and Laboratory Medicine (CCLM)

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microRNAs (miRNAs) are small non-coding RNAs that control gene expression posttranscriptionally and are part of the giant non codifying genoma. Cumulating data suggest that miRNAs are promising potential biomarkers for many diseases, including cancer. Prostate cancer (PCa) detection is currently based in the serum prostate-specific antigen biomarker and digital rectal examination. However, these methods are limited by a low predictive value and the adverse consequences associated with overdiagnosis and overtreatment. New biomarkers that could be used for PCa detection and prognosis are still needed. Recent studies have demonstrated that aberrant expressions of microRNAs are associated with the underlying mechanisms of PCa. This review attempts to extensively summarize the current knowledge of miRNA expression patterns, as well as their targets and involvement in PCa pathogenesis. We focused our review in the value of circulating and urine miRNAs as biomarkers in PCa patients, highlighting the existing discrepancies between different studies, probably associated with the important methodological issues related to their quantitation and normalization. The majority of studies have been performed in serum or plasma, but urine obtained after prostate massage appears as a new way to explore the usefulness of miRNAs. Large screening studies to select a miRNA profile have been completed, but bioinformatics tools appear as a new approach to select miRNAs that are relevant in PCa development.Promising preliminary results were published concerning miR-141, miR-375 and miR-21, but larger and prospective studies using standardized methodology are necessary to define the value of miRNAs in the detection and prognosis of PCa.

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MiR-221 promotes the development of androgen independence in prostate cancer cells via downregulation of HECTD2 and RAB1A

Cited by 131 publications

References 49 publications

miR-222 regulates sorafenib resistance and enhance tumorigenicity in hepatocellular carcinoma

miR-222 regulates sorafenib resistance and enhance tumorigenicity in hepatocellular carcinoma

Propofol suppresses proliferation and invasion of gastric cancer cells via downregulation of microRNA-221 expression

miRNAs as novel biomarkers in the management of prostate cancer

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