Psmc2, Proteasome 26S subunit, ATPase 2, is an essential part of the 19S regulatory complex of the 26S proteasome. It catalyzes the unfolding and transport of substrates into the 20S proteasome, playing a crucial role in proteasome-mediated protein degradation, which is involved in multiple cellular processes such as cell cycle regulation, apoptosis, and DNA damage repair [6]. Gene knockout or knockdown models are valuable for studying its functions.

Knockdown of Psmc2 has been shown to have significant impacts in various cancers. In oral squamous cell carcinoma (OSCC), Psmc2 knockdown inhibited cell proliferation, migration, and promoted apoptosis via the PI3K/Akt pathway, suppressing tumor growth [1]. In glioma, it inhibited cell proliferation and promoted apoptosis, and in skin cutaneous melanoma, it suppressed tumor progression by inhibiting cell proliferation, migration, DNA damage, and inducing apoptosis and cell cycle arrest [2,3]. Similar anti-tumor effects were observed in gastric cancer, nasopharyngeal carcinoma, hepatocellular carcinoma, ovarian cancer, and pancreatic cancer, with Psmc2 knockdown affecting cell growth, apoptosis, and migration through various pathways like RPS15A/mTOR, AKT, and by regulating related proteins [4,5,7,8,9].

In conclusion, Psmc2 plays a critical role in promoting the progression of multiple cancers by regulating cell growth, apoptosis, and migration. Studies using Psmc2 knockdown models have revealed its oncogenic functions in various disease areas, suggesting that targeting Psmc2 could be a potential therapeutic strategy for these cancers.