The long non-coding RNA TCONS_00006756 promotes renal cell carcinoma progression via APOB-mediated lipid metabolic reprogramming

RCC exhibits high morbidity and mortality, with lipid metabolic dysregulation driving tumor progression. lncRNAs regulate tumorigenesis and metabolism, yet the function of lncRNA TCONS_00006756 in RCC remains unknown. This study aimed to explore whether TCONS_00006756 affects RCC progression by targeting APOB and regulating lipid metabolism, to identify novel diagnostic and therapeutic targets. HK-2 (normal renal epithelial) and A498 and ACHN (RCC) cells were transfected with TCONS_00006756 shRNA. RT-PCR was used to measure TCONS_00006756, APOB, and lipid metabolism genes (FASN, ACC), while protein and EMT markers were assessed by Western blot. TCONS_00006756 and APOB were upregulated in A498 and ACHN cells versus HK-2. TCONS_00006756 knockdown suppressed RCC cell proliferation, colony formation, migration, and invasion, while inducing apoptosis and G0/G1 cell cycle arrest. TCONS_00006756 silencing downregulated key lipid synthesis enzymes FASN and ACC, indicating suppression of lipid metabolism. TCONS_00006756 knockdown reversed EMT, increasing E-Cadherin and decreasing N-Cadherin and Vimentin, via APOB regulation. TCONS_00006756 is elevated in RCC and drives tumor progression by modulating APOB-mediated lipid metabolism. It influences proliferation, invasion, EMT, and lipid reprogramming, positioning the TCONS_00006756–APOB axis as a potential therapeutic and prognostic target.