Csnk2a1, also known as casein kinase 2 alpha 1, is an important gene involved in multiple biological processes. It is known to participate in various signaling pathways, such as the PI3K-Akt-mTOR signaling pathway [2,5]. CSNK2A1 has been shown to be involved in tumorigenesis by enhancing several oncogenic signaling pathways in various cancers [2].

In pancreatic ductal adenocarcinoma (PDAC), targeted silencing of CSNK2A1 expression significantly enhances sensitivity of PDAC cells to gemcitabine treatment, as CSNK2A1 acts as a key regulator conferring gemcitabine resistance via inducing autophagy [1]. In gastric cancer, silencing CSNK2A1 expression effectively inhibits its oncogenic function, and CSNK2A1 promotes gastric cancer invasion through the PI3K-Akt-mTOR signaling pathway [2]. In cervical cancer, CSNK2A1-mediated phosphorylation of HMGA2 modulates cisplatin resistance, and inhibition of CSNK2A1 can sensitize tumor cells to cisplatin [3]. In osteosarcoma, knockdown of CSNK2A1 potentiates the cytotoxic effects of doxorubicin, as CSNK2A1 induces resistance to doxorubicin through SIRT6-mediated activation of the DNA damage repair pathway [4].

In conclusion, CSNK2A1 plays crucial roles in cancer-related biological processes, especially in drug resistance in various cancers such as PDAC, gastric cancer, cervical cancer, and osteosarcoma. The findings from loss-of-function experiments in these contexts help to understand its functions and suggest potential therapeutic strategies targeting CSNK2A1 for treating these cancers.