Molecular characterization of a novel androgen receptor transgene responsive to MicroRNA mediated post-transcriptional control exerted via 3′-untranslated region

Ebron, Jey Sabith; Shukla, Girish C.

doi:10.1002/pros.23174

Cited by 4 publications

(3 citation statements)

References 62 publications

(83 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Hence, the expression of miR-101 changes upon androgen treatment. Ebron & Shukla (2016) also found that overexpression of miR-488 mimics can repress the expression of reporters containing the 3′-UTR of AR. It has to be noted that miR-221 and miR-222 are oncogenic miRNAs as well, which are overexpressed in cancers, such as breast, pancreas, liver, and lung cancer.…”

Section: Androgen Receptormentioning

confidence: 89%

“…This variant is a result of a "gain of function" mutation and a potential mechanism of the resistance development to second-generation AR antagonists, such as abiraterone and enzalutamide. Accordingly, AR-related miRNAs could have a role in drug resistance in PCa (Table 1; Ebron & Shukla, 2016). For example, miR-1 is known as a tumor suppressor and a regulator of metastatic PCa.…”

Section: Androgen Receptormentioning

confidence: 99%

See 1 more Smart Citation

Androgen receptor‐related micro RNAs in prostate cancer and their role in antiandrogen drug resistance

Rezaei

Mahjoubin‐Tehran

Sahebkar

et al. 2019

Journal Cellular Physiology

View full text Add to dashboard Cite

Prostate cancer (PCa) is one of the most common cancers and the fifth most common reason for cancer deaths in the males. Surgical castration combined with androgen deprivation therapy, antiandrogens, and androgen synthesis inhibitors is the current therapeutic modalities for PCa. These strategies inhibit androgen synthesis or reduce its binding to the androgen receptor (AR) but the development of resistance to these therapies and transient responsiveness are challenging issues in the treatment of this cancer. Deregulation of ARs has a vital role in the initiation and progression of PCa. Also, recent findings imply that micro RNAs (miRNAs) are involved in the evolution of PCa and mediate drug resistance in different cancers. Hence, discovering and targeting miRNAs might represent a novel therapeutic approach. This review paid particular attention to the AR pathway and existing information on the possible roles of miRNAs associated with AR pathway and drug resistance to two second-generation antiandrogens, that is, enzalutamide and abiraterone.

show abstract

Section: Androgen Receptormentioning

confidence: 89%

Section: Androgen Receptormentioning

confidence: 99%

Androgen receptor‐related micro RNAs in prostate cancer and their role in antiandrogen drug resistance

Rezaei

Mahjoubin‐Tehran

Sahebkar

et al. 2019

Journal Cellular Physiology

View full text Add to dashboard Cite

show abstract

“…13,14 Certain miRNAs have been shown to regulate tumor progression via binding to the AR 3ʹ-UTR sequence. [15][16][17] As the expression of miRNAs is associated with HCC progression and metastasis, [18][19][20] and AR might promote HCC cell proliferation, it would be interesting to determine if miRNAs serve as AR upstream regulators to alter HCC cell proliferation. Bioinformatic analyses from literature and online databases (TargetScan, miRDB, and MicroCosm Targets) suggest that a subset of miRNAs, including miR-99b-5p, miR-101-3p, miR-135b-5p, miR-373-3p, and miR-375, may target the AR 3ʹ-UTR sequence and simultaneously inhibit HCC progression.…”

Section: Introductionmentioning

confidence: 99%

<p>miR-135b-5p Suppresses Androgen Receptor-Enhanced Hepatocellular Carcinoma Cell Proliferation via Regulating the HIF-2α/c-Myc/P27 Signals in vitro</p>

Bao¹,

Wang²,

Jin³

et al. 2020

OTT

View full text Add to dashboard Cite

Introduction: Hepatocellular carcinoma (HCC) accounts for more than 90% of liver cancers and is ranked as the fifth most common malignancy. Androgen receptor (AR) may promote the progression of HCC at an early stage of the disease. However, this study identified miR-135b-5p as an AR upstream regulator can suppress AR protein expression and inhibit HCC proliferation, consistent with the idea that AR expression is negatively correlated with HCC progression. Methods: The target microRNAs were predicted using online databases (TargetScan, miRDB, and MicroCosm Targets). Cell proliferation ability was measured by MTT and colony formation assay. Western blot was performed to analyze the expression levels of AR, HIF-2α, c-Myc, and p27, which are related to HCC proliferation. Chromatin immunoprecipitation (ChIP) assay and luciferase reporter assay were carried out to investigate the mechanism by which miR-135b-5p decreases AR expression. Results: miR-135b-5p suppresses HCC cell proliferation and AR expression. Downregulation of AR expression by miR-135b-5p may in turn transcriptionally modulate HIF-2α expression via direct binding of AR to the androgen response element (ARE) in the HIF-2α promoter. Further dissection of the mechanism revealed that AR-modulated HIF-2α could suppress c-Myc expression resulting in increased p27 expression that likely contributes to the suppression of proliferation in HCC cells. Conclusion: miR-135b-5p suppresses HCC cell proliferation via targeting AR-modulated HIF-2α/c-Myc/p27 signals, which may help to develop more effective therapies to prevent HCC progression.

show abstract

microRNA Analysis in Prostate Cancer

Enokida

2018

Hormone Therapy and Castration Resistance of Prostate Cancer

View full text Add to dashboard Cite

Molecular characterization of a novel androgen receptor transgene responsive to MicroRNA mediated post-transcriptional control exerted via 3′-untranslated region

Cited by 4 publications

References 62 publications

Androgen receptor‐related micro RNAs in prostate cancer and their role in antiandrogen drug resistance

Androgen receptor‐related micro RNAs in prostate cancer and their role in antiandrogen drug resistance

<p>miR-135b-5p Suppresses Androgen Receptor-Enhanced Hepatocellular Carcinoma Cell Proliferation via Regulating the HIF-2α/c-Myc/P27 Signals in vitro</p>

microRNA Analysis in Prostate Cancer

Contact Info

Product

Resources

About