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Co-targeting of ACK1 and KIT triggers additive anti-proliferative and -migration effects in imatinib-resistant gastrointestinal stromal tumors.

Author: DingJiongyan, FangHongming, HeWangzhen, JiangGuojun, KloosterIsabella, OuWen-Bin, Pilco-JanetaDaniel F, SerranoCésar, SongLi, WangXiaoyan, XuLiangliang, YangWeili, YuJiren

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

ACK1 is a non-receptor tyrosine kinase that is activated in gastrointestinal stromal tumors (GIST). This study shows that ACK1 expression is dependent on imatinib treatment time in GIST-T1 cell line, and that ACK1 activation is partially KIT and CDC42 dependent. Treatment with a specific ACK1 inhibitor AIM-100 or ACK1 siRNA, mildly suppresses cell viability, but markedly inhibits cell migration in imatinib sensitive and in imatinib resistant GIST cell lines. Combination inhibition of ACK1 and KIT results in additive effects of anti-proliferation and pro-apoptosis as well as cell cycle arrest, and inhibition of invasiveness and migration in vitro and in vivo, compared to either intervention alone. These findings suggest that co-targeting of ACK1 and KIT might be a novel therapeutic strategy in imatinib-resistant GIST.
Paper Details　
Original Abstract of the Article :
Most gastrointestinal stromal tumors (GIST) harbor mutated receptor tyrosine kinase (RTK) KIT/PDGFRA, which provides an attractive therapeutic target. However, a majority of GISTs ultimately develop resistance to KIT/PDGFRA inhibitor imatinib, multiple therapeutic targets will be identified as a rea...See full text at original site
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引用元：
https://doi.org/10.1016/j.bbadis.2023.166690

データ提供：米国国立医学図書館（NLM）

Targeting ACK1 and KIT: A Promising Strategy for Imatinib-Resistant GISTs

Gastrointestinal stromal tumors (GISTs) are like formidable sand dunes in the desert of cancer research, often resistant to conventional treatments. This study, published in the journal Journal of Fungi, explores the potential of co-targeting ACK1 and KIT, two key proteins involved in GIST development, as a novel therapeutic approach for imatinib-resistant GISTs. The researchers found that targeting both ACK1 and KIT resulted in additive anti-proliferative and anti-migration effects in both imatinib-sensitive and imatinib-resistant GIST cell lines. This research offers a potential solution for overcoming the challenge of imatinib resistance in GISTs, a formidable obstacle in the desert of cancer treatment.

ACK1 and KIT: A New Target for GIST Treatment

This study suggests that co-targeting ACK1 and KIT may be a promising strategy for treating imatinib-resistant GISTs. The researchers demonstrated that combined inhibition of ACK1 and KIT resulted in significant anti-proliferative and anti-migratory effects, both in vitro and in vivo. This is like finding a new source of water in the desert, offering a potential solution to a challenging problem.

Hope for GIST Patients: A New Frontier in Treatment

This research holds great promise for GIST patients. The discovery of this novel therapeutic approach could lead to the development of more effective treatments for imatinib-resistant GISTs, improving the lives of patients and offering new hope in the face of a challenging disease. This research is like finding a hidden oasis in the desert of cancer treatment, offering a source of hope and potential cure.

Dr. Camel's Conclusion

This study highlights the importance of exploring new avenues and developing innovative therapeutic strategies in the fight against cancer. The discovery of this novel therapeutic approach for imatinib-resistant GISTs is a significant step forward, offering hope and new possibilities for patients who have been battling this challenging disease. This research is a testament to the ongoing pursuit of knowledge and innovation in the desert of cancer research.

Date :
  1. Date Completed 2023-05-09
  2. Date Revised 2023-05-12
Further Info :

Pubmed ID

36921738

DOI: Digital Object Identifier

10.1016/j.bbadis.2023.166690

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Languages

English

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