ArticleCancer research2013
ABL regulation by AXL promotes cisplatin resistance in esophageal cancer.
Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 88 citations in OpenAlex.
- Discovery of potential AXL inhibitors using virtual screening, molecular docking, molecular dynamics, molecular mechanics, and in vitro validation.Scientific reports · 2026Article
- AXL-Mediated Drug Resistance in ALK-Rearranged NSCLC Enhanced by GAS6 From Macrophages and MMP11 Positive Fibroblasts.Cancer science · 2025Article
- Targeting AXL Inhibits the Growth and Metastasis of Prostate Cancer in Bone.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- AXL signaling in cancer: from molecular insights to targeted therapies.Signal transduction and targeted therapy · 2025Review
- Article
- Identification of a novel DNA repair inhibitor using an in silico driven approach shows effective combinatorial activity with genotoxic agents against multidrug-resistant Escherichia coli.Protein science : a publication of the Protein Society · 2024Article
- AXL in cancer: a modulator of drug resistance and therapeutic target.Journal of experimental & clinical cancer research : CR · 2023Review
- Amuvatinib Blocks SARS-CoV-2 Infection at the Entry Step of the Viral Life Cycle.Microbiology spectrum · 2023Article
- Bioactive Compounds from the Mushroom-Forming FungusAntibiotics (Basel, Switzerland) · 2023Article
- Altered expression of AXL receptor tyrosine kinase in gastrointestinal cancers: a promising therapeutic target.Frontiers in oncology · 2023Review
- Article
- Regulation of the Receptor Tyrosine Kinase AXL in Response to Therapy and Its Role in Therapy Resistance in Glioblastoma.International journal of molecular sciences · 2022Article
- AXL Promotes Metformin-Induced Apoptosis Through Mediation of Autophagy by Activating ROS-AMPK-ULK1 Signaling in Human Esophageal Adenocarcinoma.Frontiers in oncology · 2022Article
- Anti-Axl monoclonal antibodies attenuate the migration of MDA-MB-231 breast cancer cells.Oncology letters · 2021Article
- Subcritical Water Extracts fromJournal of fungi (Basel, Switzerland) · 2021Article
- Inhibition of AXL enhances chemosensitivity of human ovarian cancer cells to cisplatin via decreasing glycolysis.Acta pharmacologica Sinica · 2021Article
- Targeted Molecular Therapies in the Treatment of Esophageal Adenocarcinoma, Are We There Yet?Cancers · 2020Review
- Review
- AXL Mediates Cetuximab and Radiation Resistance Through Tyrosine 821 and the c-ABL Kinase Pathway in Head and Neck Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- Co-overexpression of AXL and c-ABL predicts a poor prognosis in esophageal adenocarcinoma and promotes cancer cell survival.Journal of Cancer · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Esophageal adenocarcinoma (EAC) is characterized by resistance to chemotherapy and poor outcome. Although cisplatin (CDDP) has been used as a first-line therapy in patients with EAC, resistance remains a major clinical problem. The AXL receptor tyrosine kinase, originally isolated as a transforming gene from leukemia, is overexpressed in several solid tumors. Herein, we assessed AXL protein expression in human EACs and examined its role in CDDP resistance in human EAC cells. AXL overexpression was detected in more than 50% of tumors examined. Elevating AXL in nonoverexpressing cells doubled the CDDP IC(50) and increased cell survival three-fold, while attenuating AXL in overexpressing cells reduced survival two-fold. The effects of AXL modulation on cell survival were associated with changes in cellular and molecular markers of apoptosis. Mechanistic investigations revealed that AXL blocked CDDP-induced activation of endogenous p73β (TP73), reducing its protein half-life, and inhibited CDDP-induced levels of p-c-ABL(Y412) and p-p73β(Y99). These changes were associated with a disruption of c-ABL/p73β protein interactions due to association with c-ABL in the cytoplasm, thereby blocking nuclear accumulation of c-ABL and phosphorylation of p73β in response to DNA damage. Together, our results establish that AXL promotes CDDP resistance in esophageal adenocarcinoma and argue that therapeutic targeting of AXL may sensitize these cancers to DNA-damaging drugs.
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