ArticleOncogene2014
MiR-221 promotes the development of androgen independence in prostate cancer cells via downregulation of HECTD2 and RAB1A.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
73 citing papers in PubMed, 1 synthesis or guideline pooled it, 147 citations in OpenAlex.
- Pooled analysis of prognostic value and clinical significance of Rab1A expression in human solid tumors.Medicine · 2019Pooled it
- Genomic landscape and precision therapy in prostate cancer: current status and future directions.NPJ precision oncology · 2026Review
- Article
- Lactylation-Driven HECTD2 Limits the Response of Hepatocellular Carcinoma to Lenvatinib.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Expression of HECTD2 predicts peritoneal metastasis of gastric cancer and reconstructs immune microenvironment.Cancer cell international · 2024Article
- The 'Other' subfamily of HECT E3 ubiquitin ligases evaluate the tumour immune microenvironment and prognosis in patients with hepatocellular carcinoma.IET systems biology · 2024Article
- Molecular landscape for risk prediction and personalized therapeutics of castration-resistant prostate cancer: at a glance.Frontiers in endocrinology · 2024Review
- Exosomal miR-222-3p contributes to castration-resistant prostate cancer by activating mTOR signaling.Cancer science · 2023Article
- Deregulated microRNAs Involved in Prostate Cancer Aggressiveness and Treatment Resistance Mechanisms.Cancers · 2023Review
- Transcriptome Profiling of Prostate Cancer, Considering Risk Groups and the TMPRSS2-ERG Molecular Subtype.International journal of molecular sciences · 2023Article
- Molecular Mechanisms of Noncoding RNA in the Occurrence of Castration-Resistant Prostate Cancer.International journal of molecular sciences · 2023Review
- Ki-67, topoisomerase IIα and miR-221 have a limited prostate cancer risk stratification ability on a medium-term follow-up: results of a high-risk radical prostatectomy cohort.Translational andrology and urology · 2022Article
- miR-221/222 as biomarkers and targets for therapeutic intervention on cancer and other diseases: A systematic review.Molecular therapy. Nucleic acids · 2022Review
- Liver and Kidney Surgical Anatomy to Verify the Effect of miR-221 on Organ Damage in Septic Rats.Journal of healthcare engineering · 2022Article
- Interaction between Non-Coding RNAs and Androgen Receptor with an Especial Focus on Prostate Cancer.Cells · 2021Review
- Wnt/β-catenin signal transduction pathway in prostate cancer and associated drug resistance.Discover oncology · 2021Review
- Article
- Rab1A promotes cell proliferation and migration by upregulating Gli1 in colorectal cancer.Scientific reports · 2021Article
- HIF-1α Induces HECTD2 Up-Regulation and Aggravates the Malignant Progression of Renal Cell CancerFrontiers in cell and developmental biology · 2021Article
- Review
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
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 of the CRPC phenotype. In current study, we show that stably overexpressing miR-221 confers androgen independent (AI) cell growth in LNCaP by rescuing LNCaP cells from growth arrest at G1 phase due to the lack of androgen. Overexpressing of miR-221 in LNCaP reduced the transcription of a subgroup of androgen-responsive genes without affecting the androgen receptor (AR) or AR-androgen integrity. By performing systematic biochemical and bioinformatical analyses, we identified two miR-221 targets, HECTD2 and RAB1A, which could mediate the development of CRPC phenotype in multiple prostate cancer cell lines. Downregulation of HECTD2 significantly affected the androgen-induced and AR-mediated transcription, and downregulation of HECTD2 or RAB1A enhances AI cell growth. As a result of the elevated expression of miR-221, expression of many cell cycle genes was altered and pathways promoting epithelial to mesenchymal transition/tumor metastasis were activated. We hypothesize that a major biological consequence of upregulation of miR-221 is reprogramming of AR signaling, which in turn may mediate the transition to the CRPC phenotype.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.