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Inhibition of androgen receptor enhanced the anticancer effects of everolimus through targeting glucose transporter 12.

Author: CaoBo, ChenLin, GaoJingwang, LiHanghang, WeiBo, XuXingming, ZhaoRuiyang

Journal ArticleAn article published in an academic or professional journal that reports original research or scholarly analysis.
Research Support, Non-U.S. Gov'tResearch funding provided by government agencies outside the United States.

Overview

Everolimus, an mTOR inhibitor, is a targeted drug for gastric cancer (GC) therapy. This study investigated the mechanisms of response to everolimus and developed novel regimens for GC treatment. The study found that everolimus inhibits glycolysis in GC cells in a dose-dependent manner. However, GLUT12, a glucose transporter, was upregulated to counteract the anticancer effects of everolimus. Inhibition of androgen receptor (AR) activity, which promotes GLUT12 expression, or GLUT12 knockdown enhanced the anticancer effects of everolimus. These findings suggest that targeting the AR/GLUT12 pathway may improve the efficacy of everolimus in GC therapy.
Paper Details　
Original Abstract of the Article :
Everolimus was designed as a mammalian target of rapamycin (mTOR) inhibitor. It has been proven as a targeted drug for gastric cancer (GC) therapy. However, long-term treatment with everolimus may cause severe side effects for recipients. Decreasing the dosage and attenuating the associated risks ar...See full text at original site
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引用元：
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9760431/

データ提供：米国国立医学図書館（NLM）

Androgen Receptor Inhibition: A Novel Approach for Enhancing Everolimus Efficacy

This study investigates the potential of inhibiting the androgen receptor (AR) to enhance the anticancer effects of everolimus, a mammalian target of rapamycin (mTOR) inhibitor, in gastric cancer (GC). The research explores the mechanisms underlying everolimus-induced apoptosis and glycolysis inhibition, identifying the role of glucose transporter 12 (GLUT12) in counteracting everolimus efficacy. The study demonstrates that inhibiting AR activity can suppress GLUT12 expression, augmenting the anticancer effects of everolimus. This study contributes to the development of more effective and personalized treatment strategies for GC, potentially improving patient outcomes and extending survival.

Androgen Receptor Inhibition: A New Strategy for Tailoring Gastric Cancer Treatment

This study unveils a novel strategy for enhancing the efficacy of everolimus, a mammalian target of rapamycin (mTOR) inhibitor, in gastric cancer (GC) treatment. The findings highlight the importance of targeting the androgen receptor (AR) to suppress GLUT12 expression and potentiate the anticancer effects of everolimus. This research paves the way for more effective and personalized treatment strategies for GC, offering hope for improved patient outcomes and extended survival.

Androgen Receptor Inhibition: A New Oasis in the Desert of Gastric Cancer Treatment

The desert of gastric cancer treatment can be a challenging landscape, often plagued by resistance and limited therapeutic options. This study presents a new oasis of hope, highlighting the potential of inhibiting the androgen receptor (AR) to enhance the efficacy of everolimus, a mammalian target of rapamycin (mTOR) inhibitor. The findings suggest that targeting the AR/GLUT12 pathway can lead to more effective and personalized treatment strategies for GC, potentially improving patient outcomes and extending survival.

Dr.Camel's Conclusion

This study investigates the potential of inhibiting the androgen receptor (AR) to enhance the anticancer effects of everolimus, a mammalian target of rapamycin (mTOR) inhibitor, in gastric cancer (GC). The research explores the mechanisms underlying everolimus-induced apoptosis and glycolysis inhibition, identifying the role of glucose transporter 12 (GLUT12) in counteracting everolimus efficacy. The study demonstrates that inhibiting AR activity can suppress GLUT12 expression, augmenting the anticancer effects of everolimus. This study contributes to the development of more effective and personalized treatment strategies for GC, potentially improving patient outcomes and extending survival.
Date :
  1. Date Completed 2023-01-09
  2. Date Revised 2023-02-06
Further Info :

Pubmed ID

36594084

DOI: Digital Object Identifier

PMC9760431

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Languages

English

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