Cct6a, short for Chaperonin Containing TCP1 Subunit 6A, is a molecular chaperone involved in the folding and stabilization of newly synthesized proteins. It participates in multiple biological processes and is associated with various pathways, highlighting its significance in maintaining cellular functions. Genetic models, such as knockout (KO) mouse models, are valuable for studying its functions [1-10].

In multiple cancers, Cct6a has been shown to play a promoting role. In lung adenocarcinoma, CCT6A silencing inhibited cell proliferation, migration, and increased apoptosis rates. It interacted with STAT1, protecting it from ubiquitination-mediated degradation, thus enhancing the transcription of HK2 and promoting aerobic glycolysis [1]. In osteosarcoma, CCT6A knockdown attenuated cell growth, viability, and survival, and induced apoptosis and cell cycle arrest at G0/G1 phases, also suppressing the Akt pathway [2]. In colon cancer, CCT6A silencing suppressed proliferation and survival, and CCT6A influenced BIRC5 through different pathways depending on p53 status [3]. In esophageal squamous cell carcinoma, CCT6A knockdown inhibited cell proliferation, invasion, and epithelial-mesenchymal transition, while overexpression had opposite effects, and it activated the TGF-β/Smad/c-Myc pathway [4].

In conclusion, Cct6a is a crucial gene in protein folding and stabilization. Through model-based research, it has been found to play important roles in cancer-related biological processes such as cell proliferation, apoptosis, and metabolic reprogramming. These findings contribute to understanding the mechanisms of cancer development and suggest Cct6a as a potential therapeutic target in cancers like lung adenocarcinoma, osteosarcoma, colon cancer, and esophageal squamous cell carcinoma.