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Elucidating the molecular basis of ATP-induced cell death in breast cancer: Construction of a robust prognostic model    

文献类型:期刊文献

英文题名:Elucidating the molecular basis of ATP-induced cell death in breast cancer: Construction of a robust prognostic model

作者:Zhang, Hao-Ling[1];Doblin, Sandai[1,10];Zhang, Zhong-Wen[2];Song, Zhi-Jing[3];Dinesh, Babu[4];Tabana, Yasser[4];Saad, Dahham Sabbar[5];Adam, Mowaffaq Adam Ahmed;Wang, Yong[6];Wang, Wei[7];Zhang, Hao-Long[8];Wu, Sen[9];Zhao, Rui[3];Khaled, Barakat[4]

第一作者:Zhang, Hao-Ling

通信作者:Doblin, S[1]

机构:[1]Univ Sains Malaysia, Adv Med & Dent Inst, Dept Biomed Sci, George Town 13200, Malaysia;[2]Gansu Univ Chinese Med, Sch Publ Hlth, Lanzhou 730000, Gansu, Peoples R China;[3]Gansu Univ Chinese Med, Clin Coll Chinese Med, Lanzhou 730000, Gansu, Peoples R China;[4]Univ Alberta, Fac Pharm & Pharmaceut Sci, Edmonton, AB T6G 2E1, Canada;[5]Univ Technol & Appl Sci Rustaq, Dept Sci, Rustaq 10, Oman; San Diego State Univ, Dept Chem & Biochem, San Diego, CA 92182 USA;[6]Gansu Univ Chinese Med, Dept Pathol Ctr, Lanzhou 730000, Gansu, Peoples R China;[7]Gansu Univ Chinese Med, Coll Acupuncture Moxibust & Tuina, Lanzhou 730000, Gansu, Peoples R China;[8]Univ Sains Malaysia, Adv Med & Dent Inst, George Town 13200, Malaysia;[9]Univ Sains Malaysia, Dept Biomed Sci, George Town 13200, Malaysia;[10]Univ Sains Malaysia, Adv Med & Dent Inst, Dept Biomed Sci, Kepala Batas 13200, Penang, Malaysia

第一机构:Univ Sains Malaysia, Adv Med & Dent Inst, Dept Biomed Sci, George Town 13200, Malaysia

通信机构:[1]corresponding author), Univ Sains Malaysia, Adv Med & Dent Inst, Dept Biomed Sci, Kepala Batas 13200, Penang, Malaysia.

年份:2024

卷号:15

期号:2

外文期刊名:WORLD JOURNAL OF CLINICAL ONCOLOGY

收录:WOS:【ESCI(收录号:WOS:001181241600004)】;

基金:2Supported by National Natural Science Foundation of China, No. 81960877; University Innovation Fund of Gansu Province, No. 2021A-076; Gansu Province Science and Technology Plan (Innovation Base and Talent Plan), No. 21JR7RA561; Natural Science Foundation of Gansu Province, No. 21JR1RA267 and No. 22JR5RA582; Education Technology Innovation Project of Gansu Province, No. 2022A-067; Innovation Fund of Higher Education of Gansu Province, No. 2023A-088; Gansu Province Science and Technology Plan International Cooperation Field Project, No. 23YFWA0005; and Open Project of Key Laboratory of Dunhuang Medicine and Transformation of Ministry of Education, No. DHYX21-07, No. DHYX22-05, and No. DHYX21-01.

语种:英文

外文关键词:ATP-induced cell death; mRNA; miRNA; Prognostic model; Breast cancer

摘要:BACKGROUND Breast cancer is a multifaceted and formidable disease with profound public health implications. Cell demise mechanisms play a pivotal role in breast cancer pathogenesis, with ATP-triggered cell death attracting mounting interest for its unique specificity and potential therapeutic pertinence. AIM To investigate the impact of ATP-induced cell death (AICD) on breast cancer, enhancing our understanding of its mechanism. METHODS The foundational genes orchestrating AICD mechanisms were extracted from the literature, underpinning the establishment of a prognostic model. Simultaneously, a microRNA (miRNA) prognostic model was constructed that mirrored the gene-based prognostic model. Distinctions between high- and low-risk cohorts within mRNA and miRNA characteristic models were scrutinized, with the aim of delineating common influence mechanisms, substantiated through enrichment analysis and immune infiltration assessment. RESULTS The mRNA prognostic model in this study encompassed four specific mRNAs: P2X purinoceptor 4, pannexin 1, caspase 7, and cyclin 2. The miRNA prognostic model integrated four pivotal miRNAs: hsa-miR-615-3p, hsa-miR-519b-3p, hsa-miR-342-3p, and hsa-miR-324-3p. B cells, CD4+ T cells, CD8+ T cells, endothelial cells, and macrophages exhibited inverse correlations with risk scores across all breast cancer subtypes. Furthermore, Kyoto Encyclopedia of Genes and Genomes analysis revealed that genes differentially expressed in response to mRNA risk scores significantly enriched 25 signaling pathways, while miRNA risk scores significantly enriched 29 signaling pathways, with 16 pathways being jointly enriched. CONCLUSION Of paramount significance, distinct mRNA and miRNA signature models were devised tailored to AICD, both potentially autonomous prognostic factors. This study's elucidation of the molecular underpinnings of AICD in breast cancer enhances the arsenal of potential therapeutic tools, offering an unparalleled window for innovative interventions. Essentially, this paper reveals the hitherto enigmatic link between AICD and breast cancer, potentially leading to revolutionary progress in personalized oncology.

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