BIT1 as an Effector of EGFR-TKI-induced Apoptosis <i>via</i> TLE1 Inhibition in Lung Adenocarcinoma Cells

The Bit1/TLE1 axis is a pivotal regulatory switch dictating apoptotic outcomes following EGFR-TKI treatment. This mechanism identifies a therapeutic vulnerability, suggesting that pharmacological Bit1 pathway activation could be an effective strategy to overcome acquired resistance in LUAD.

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Publication Details

Journal
Anticancer Research
Published
2026-03-27
DOI
https://doi.org/10.21873/anticanres.18075
Primary Topic
Lung Cancer Treatments and Mutations
Type
article
Field-Weighted Citation Impact
0.00
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article

BIT1 as an Effector of EGFR-TKI-induced Apoptosis via TLE1 Inhibition in Lung Adenocarcinoma Cells

Xin Yao, Hector Biliran, Renwei Chen, James Bailey et al.
Anticancer Research
Lung Cancer Treatments and Mutations
article

BIT1 as an Effector of EGFR-TKI-induced Apoptosis via TLE1 Inhibition in Lung Adenocarcinoma Cells

Xin Yao, Hector Biliran, Renwei Chen, James Bailey, Ma. Carmela Dela Cruz, Alajah Nealy, PAUL MARK MEDINA, MICAH NALLS
article en

Abstract

The Bit1/TLE1 axis is a pivotal regulatory switch dictating apoptotic outcomes following EGFR-TKI treatment. This mechanism identifies a therapeutic vulnerability, suggesting that pharmacological Bit1 pathway activation could be an effective strategy to overcome acquired resistance in LUAD.

Anticancer ResearchVol. 46(4)
University of California, Santa Barbara (US), Xavier University of Louisiana (US), University of the Philippines Manila (PH)
Reduced inequalities
Openalex Percentile: Top 6%
Lung Cancer Treatments and Mutations
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