HOXC9 promotes cell proliferation and suppresses mitochondria-mediated apoptosis through the AKT/mTOR signaling pathway in esophageal squamous cell carcinoma
Homeobox C9 (HOXC9) is aberrantly expressed in multiple malignancies; however, its functional role in esophageal squamous cell carcinoma (ESCC) remains elusive. This study investigated the expression, function, and underlying molecular mechanisms of HOXC9 in ESCC. Based on the experimental data, we hypothesized that HOXC9 may contribute to ESCC initiation and progression by promoting cell proliferation and suppressing mitochondria-dependent apoptosis. To elucidate the underlying molecular mechanism, we conducted KEGG pathway enrichment analysis of transcriptomic data from HOXC9-knockdown cells, with results visualized using dot and bar plots.Esophageal cancer cells were transfected with HOXC9-specific siRNA or negative control (NC) siRNA and cultured for 24-48 h. Approximately 1 x 10^7 cells were then collected and lysed in RNase-free microcentrifuge tubes using TRIzol reagent (Life Technologies). Total RNA was extracted and subjected to RNA sequencing (RNA-Seq) by Novogene Co., Ltd. (Beijing, China). KEGG pathway enrichment analysis was subsequently performed on the transcriptomic data. The enriched pathways provided functional annotation that concretely linked HOXC9 knockdown (genotype) to the phenotypic outcomes, specifically the inhibition of cell proliferation and the promotion of mitochondria-dependent apoptosis. These pathways thus served as the mechanistic bridge between the genetic perturbation and the observed cellular phenotypes.