PPA1, TRIM68 and FBXO46: Potential Therapeutic Targets for Triple Negative Breast Cancer

三阴性乳腺癌 乳腺癌 医学 肿瘤科 内科学 癌症
作者
Fatima Haider,Nida Syed,Syeda Abiha Zehra Jaffari,Basir Syed,Aftab Ahmed,Shamshad Zarina,Zehra Hashim
出处
期刊:Current Protein & Peptide Science [Bentham Science Publishers]
卷期号:26
标识
DOI:10.2174/0113892037334325241014053319
摘要

Background: Triple-negative breast cancer (TNBC) is an aggressive type of breast cancer with a high recurrence rate. A new therapeutic intervention is urgently needed to combat this lethal subtype. The identification of biomarkers is also crucial for improving outcomes in TNBC. Method: The cell cytotoxicity of ML364 (2-(4-Methylphenylsulfonamido)-N-(4-phenylthiazol- 2-yl)-4-(trifluoromethyl)benzamide) was measured at different concentrations of ML364 in TNBC-treated and untreated cells. The 2DE and LC-MS/MS analysis were used for protein identification of differentially expressed proteins. Furthermore, the quantitation of gene expression was demonstrated using RT-qPCR. TIMER, HPA, and UALCAN databases were utilized for further analysis. Results: Differentially expressed proteins and genes after ML364 treatment in TNBC were found to be linked with the USP2 (ubiquitin specific peptidase 2)-mediated pathway. Our results demonstrate that differentially identified proteins, including PPA1, TRIM68, and FBXO46, could be a potential prognostic biomarker for TNBC. Further analysis through the UALCAN and HPA databasess showsthe high expression of these proteins in primary breast tumors, which is in contrast to normal. The induction of ML364 significantly reduced the expression of PPA1, TRIM68, and FBXO46 proteins and induced cell cytotoxicity in TNBC cells. Conclusion: This study provides an understanding of the USP2-mediated signaling pathway in TNBC, emphasizing the role of USP2 and its substrates with apoptotic genes. Our results offer insight into the USP2-mediated cellular mechanism after ML364 treatment in TNBC that could be a potential therapeutic candidate.
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