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Article

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

Oncogene - 22 May 2014

Sun T, Wang X, He H H, Sweeney C J, Liu S X, Brown M, Balk S, Lee G-Sm, Kantoff P W

Abstract excerpt

Hormone-sensitive prostate cancer typically progresses to castration resistant prostate cancer (CRPC) after the androgen deprivation therapy. We investigated the impact of microRNAs (miRs) in the transition of prostate cancer to CRPC. MiR-221/-222 was highly expressed in bone metastatic CRPC tumor specimens. We previously demonstrated that transient overexpression of miR-221/-222 in LNCaP promoted the development...

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Share to Androgens
Share to Cell Cycle
Share to Epithelial-Mesenchymal Transition

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to MicroRNAs

Share to Prostatic Neoplasms, Castration-Resistant

Share to Receptors, Androgen

Share to RNA Interference

Share to Ubiquitin-Protein Ligases

Source

Open in PubMed Open full text

Identifiers

PMID: 23770851
DOI: 10.1038/onc.2013.230
PMCID: PMC3883998

Genes

HECTD2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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MiR-221 promotes the development of androgen independence in prostate cancer cells via downregulation of HECTD2 and RAB1A.PMID 23770851Read ↗

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