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Activated MKK3/MYC crosstalk impairs dabrafenib response in BRAFV600E colorectal cancer leading to resistance.

Author: BartolazziArmando, BernardiniRoberta, BlandinoGiovanni, BossiGianluca, CarpanoSilvia, DiodoroMaria Grazia, Lo SardoFederica, MilellaMichele, PiastraValentina, PrantedaAngelina, SerraMartina

Journal ArticleAn article published in an academic or professional journal that reports original research or scholarly analysis.

Overview

This study investigated the role of MKK3 in BRAF inhibitor resistance in colorectal cancer (CRC) cells with BRAF mutations. The findings suggest that MKK3 activation contributes to resistance and that targeting MKK3 could be a promising therapeutic strategy for BRAF<sup>V600E</sup> CRC.
Paper Details　
Original Abstract of the Article :
Colorectal cancer (CRC) patients with BRAF mutations develop resistance to BRAF inhibitors at a very early stage. Understanding the molecular mechanisms involved in BRAF inhibitor resistance is critical for the development of novel therapeutic opportunities for this subtype of CRC patients. CRC cell...See full text at original site
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引用元：
https://doi.org/10.1016/j.biopha.2023.115480

データ提供：米国国立医学図書館（NLM）

Activated MKK3/MYC Crosstalk Impairs Dabrafenib Response in BRAFV600E Colorectal Cancer

The study investigates the complex world of colorectal cancer (CRC) and the challenges in treating patients with BRAF mutations. It delves into the molecular mechanisms behind BRAF inhibitor resistance, a significant hurdle in achieving effective treatment for this type of cancer. The researchers focused on the role of MKK3, a specific activator of p38MAPKs signaling, and its interaction with the MYC oncoprotein.

Unveiling Resistance Mechanisms

This research identified a novel mechanism of dabrafenib resistance in BRAFV600E CRC cells. The researchers found that activated MKK3 interacts with MYC, promoting its stability and hindering the effectiveness of dabrafenib. This groundbreaking discovery sheds light on a previously unknown vulnerability that could be targeted for future therapeutic interventions.

Targeting the Resistance

The study suggests a potential pathway for overcoming dabrafenib resistance in BRAFV600E CRC by targeting the MKK3/MYC crosstalk. This research offers valuable insights into the molecular mechanisms underlying drug resistance, paving the way for the development of personalized treatments that effectively combat cancer cells.

Dr.Camel's Conclusion

Think of CRC cells as an oasis in the vast desert, thriving on the water supplied by MKK3. The BRAF inhibitor, like a traveler, aims to dry up the oasis. But the cells have a secret weapon: a partnership with MYC, which acts like a well, constantly replenishing the water supply. This research unveils this secret partnership, offering a potential way to cut off the water source and defeat the CRC oasis.

Date :
  1. Date Completed 2023-11-07
  2. Date Revised 2023-11-07
Further Info :

Pubmed ID

37713993

DOI: Digital Object Identifier

10.1016/j.biopha.2023.115480

Related Literature

Article Analysis
・Effects of dabrafenib
SNS
PICO Info
in preparation
Languages

English

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