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ORIGINAL RESEARCH article

Front. Public Health
Sec. Radiation and Health
Volume 12 - 2024 | doi: 10.3389/fpubh.2024.1496439
This article is part of the Research Topic Advances in Radiation Research and Applications: Biology, Environment and Medicine View all articles

The role of PCBP1 in carbon ion-induced ferroptosis and inhibition of lung adenocarcinoma proliferation

Provisionally accepted
Zhen Yang Zhen Yang 1,2*ZHENCHAO KANG ZHENCHAO KANG 3XUEJIAO TIAN XUEJIAO TIAN 1YICHAO GENG YICHAO GENG 2QIUNING ZHANG QIUNING ZHANG 2YANLI LIU YANLI LIU 4Hongtao Luo Hongtao Luo 5
  • 1 School of Public Health, Gansu University of Chinese Medicine, Lanzhou, Gansu Province, China
  • 2 Institute of Modern Physics, Chinese Academy of Sciences (CAS), Lanzhou, Gansu Province, China
  • 3 Department of Radiotherapy, Liangzhou Hospital of Wuwei city, Wuwei, China., Wuwei, China
  • 4 Gansu Provincial Cancer Hospital, Lanzhou, Gansu Province, China
  • 5 Gansu Provincial Hospital of TCM, Lanzhou, Gansu Province, China

The final, formatted version of the article will be published soon.

    Objective: To investigate the role of PCBP1 in the inhibition of lung adenocarcinoma proliferation by carbon irradiation. Methods: A549 cells were irradiated with different doses of carbon ions to observe clonal survival and detect changes in cell proliferation. Whole transcriptome sequencing and the Illumina platform were used to analyze the differentially expressed genes in A549 cells after carbon ion irradiation. The relationship between the expression levels of PCBP1, ACSL4, and ALOX15 and survival was analyzed by combining data from the UCSC database and the Kaplan-Meier Plotter public platform. Additionally, the knockdown of the poly (rC)-binding protein 1 (PCBP1) gene using siRNA techniques was employed to further investigate the relationship between the expression levels of PCBP1 and ALOX15. To investigate the relationship between ALOX15 expression and survival, we assessed changes in key indicators of ferroptosis (mitochondrial morphology, ROS, MDA, and divalent iron) in A549 cells after knocking down the PCBP1 gene using siRNA technology. Additionally, the expressions of PCBP1, ACSL4, and ALOX15 in different groups were further analyzed through RT-PCR and Western blot techniques. The differential expression of PCBP1, ACSL4, and ALOX15 in NSCLC tissues was found to correlate with clinical prognosis for survival. Results: Carbon ions significantly inhibited the proliferation of A549 cells, and 5.16 Gy carbon ions significantly induced the expression of differentially expressed genes in these cells. Additionally, carbon ions inhibited the expression of PCBP1, which led to alterations in mitochondrial morphology in lung adenocarcinoma cells. This was associated with a significant increase in the levels of ROS, MDA, and Fe2+. Furthermore, low expression of PCBP1 promoted ferroptosis by increasing the expression of ACSL and ALOX15. Conclusion: Carbon ions decreased the expression of PCBP1 in A549 cells, and low expression of PCBP1 inhibited tumor proliferation by promoting ferroptosis.

    Keywords: Carbon ion, ferroptosis, PCBP1, Lung Adenocarcinoma, proliferation

    Received: 14 Sep 2024; Accepted: 21 Nov 2024.

    Copyright: © 2024 Yang, KANG, TIAN, GENG, ZHANG, LIU and Luo. 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: Zhen Yang, School of Public Health, Gansu University of Chinese Medicine, Lanzhou, 730000, Gansu Province, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.