GAPDHP65 knockout reveals its critical role in TNBC cell survival and therapeutic potential 2814

Abstract Description Background Triple-negative breast cancer (TNBC) is an aggressive subtype with limited treatment options. Dysregulated pseudogene expression is increasingly recognized in cancer progression, though many pseudogenes remain poorly characterized. This study examines GAPDHP65, a pseudogene potentially involved in TNBC growth and survival. Methods Computational analysis of gene expression profiles identified GAPDHP65 as highly expressed in TNBC compared to normal tissue. Experimental validation via qPCR confirmed differential expression. GAPDHP65 was knocked out in TNBC cells using CRISPR-Cas9, with gene editing efficiency verified by indel detection, qPCR, and sequencing. Functional assays assessed cell viability and growth to determine the impact of GAPDHP65 suppression. Results GAPDHP65 expression was elevated in TNBC cells and its knockout significantly reduced cell viability. These findings suggest that GAPDHP65 plays a critical role in TNBC progression, maintaining cancer cell survival. Conclusions This study identifies GAPDHP65 as a pseudogene with a significant role in TNBC. Its elevated expression and impact on cell survival position GAPDHP65 as a promising therapeutic target for future cancer treatments. Topic Categories Tumor Immunology: Checkpoints, Prevention, and Treatment (TIPT)