induction of akt activity by chemotherapy confers acquired resistance

Clicks: 149
ID: 183968
2009
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #190 of 246 articles by views in Bioorganic & medicinal chemistry letters

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 246 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Abstract
Resistance to chemotherapy is a major cause of treatment failure in human cancer. Accumulating evidence has indicated that the acquisition of resistance to chemotherapeutic drugs involves the activation of the PI3K/Akt pathway. Modulating Akt activity in response to chemotherapy has been observed often in chemoresistant cancers. The potential molecular mechanisms by which chemotherapeutic agents activate the PI3K/Akt pathway are emerging. Activation of this pathway evades the cytotoxic effects of chemotherapeutic agents via regulation of essential cellular functions such as protein synthesis, antiapoptosis, survival and proliferation in cancer. How chemotherapeutic agents induce Akt activation and how activated Akt confers chemoresistance through regulation of signaling networks are discussed in this review. Combining PI3K/Akt inhibitors with standard chemotherapy has been successful in increasing the efficacy of chemotherapeutic agents both in vivo and in vitro. Several small molecules have been developed to specifically target PI3K/Akt and other components of this pathway, which in combination with chemotherapy may be a valid approach to overcome therapeutic resistance. We propose several feedback and feedforward regulatory mechanisms of signaling networks for maintenance of the Akt activity for cell survival. These regulatory mechanisms may limit the efficacy of PI3K/Akt-targeted therapy; therefore, disruption of these mechanisms may be an effective strategy for development of novel anti-cancer therapies.
Reference Key
huang2009journalinduction Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Wei-Chien Huang;Mien-Chie Hung
Journal Bioorganic & medicinal chemistry letters
Year 2009
DOI
10.1016/S0929-6646(09)60051-6
URL
Keywords

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

No comments yet. Be the first to comment on this article.