ORIGINAL RESEARCH article
Front. Oncol.
Sec. Pharmacology of Anti-Cancer Drugs
Volume 15 - 2025 | doi: 10.3389/fonc.2025.1576685
Aurintricarboxylic Acid Inhibits the Malignant Phenotypes of Drug-Resistant Cells via Translational Regulation
Provisionally accepted
- Key Laboratory of Functional Protein Research of Guangdong Higher Education Institutes and MOE Key Laboratory of Tumor Molecular Biology, Institute of Life and Health Engineering,Jinan University, Guangzhou, China
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Genome instability, a hallmark of cancer, leads to endless mutations that eventually cause drug resistance against almost all chemotherapy drugs. This poses a significant obstacle to the success of cancer treatments. Here, we report that aurintricarboxylic acid (ATCA) effectively suppresses the malignant phenotypes, including proliferation, migration, invasion, and clone formation, of cancer cells of multiple cancers, including cisplatin-resistant lung cancer cells, paclitaxel-resistant lung cancer cells and doxorubicin-resistant breast cancer cells. Interestingly, ATCA does not cause acute cytotoxicity. Proteome analysis of the whole proteome, and nascent chains showed that ATCA reduced translation initiation and thus reduced the abundance of the highly abundant respiratory chain complex. This lowered the potential of the mitochondrial membrane, and thus restricted the energy production. This principle could be hardly circumvented by cancer cells, and thus may serve as a promising and universal candidate for a second-line therapeutic agent to control cancer progression after drug resistance.
Keywords: aurintricarboxylic acid (ATCA), Drug Resistance, translation inhibition, Secondline Therapeutic Agent, Malignant behavior
Received: 14 Feb 2025; Accepted: 21 Apr 2025.
Copyright: © 2025 Shang, Chen, Jin, Wang and Zhang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Tong Wang, Key Laboratory of Functional Protein Research of Guangdong Higher Education Institutes and MOE Key Laboratory of Tumor Molecular Biology, Institute of Life and Health Engineering,Jinan University, Guangzhou, China
Gong Zhang, Key Laboratory of Functional Protein Research of Guangdong Higher Education Institutes and MOE Key Laboratory of Tumor Molecular Biology, Institute of Life and Health Engineering,Jinan University, Guangzhou, China
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