LINC00942 accelerates esophageal cancer progression via NAT10/HSPD1

Long non-coding RNAs (lncRNAs) have been implicated in the progression of esophageal cancer (ESCA). This study investigates the oncogenic role of LINC00942 in ESCA, revealing its upregulation in tumor tissues and cell lines. Functional assays demonstrated that suppression of LINC00942 significantly reduced cell viability and tumor growth while promoting apoptosis both in vitro and in vivo using a xenograft tumor model. Mechanistically, LINC00942 silencing decreased NAT10 expression in ESCA cells and tumors, with NAT10 overexpression rescuing the inhibition of ESCA cell proliferation, migration, and invasion induced by LINC00942 knockdown, alongside a reduction in apoptosis and tumor growth inhibition. Notably, LINC00942 directly interacted with NAT10, which were co-localized in the nucleus. Further analysis indicated that NAT10 overexpression enhanced the stability and expression of HSPD1 through increased N4-acetylcytidine (ac4C) modification, thereby exerting its effects by interacting with HSPD1. These findings highlight the pivotal role of the LINC00942/NAT10/HSPD1 axis in ESCA development, suggesting it as a potential biomarker and therapeutic target for the disease.