Sox12, a member of the SoxC group, is a crucial transcription factor. It has been implicated in various biological processes and disease conditions. In the immune system, it is involved in T-cell differentiation pathways, and in cancer, it has been associated with multiple oncogenic signaling pathways [4,8]. Genetic models, such as gene knockout (KO) and conditional knockout (CKO) mouse models, are valuable for studying its functions.

In hepatocellular carcinoma (HCC), hepatocyte-specific Sox12 knockout attenuates DEN/CCl4-induced HCC progression and metastasis, while hepatocyte-specific Sox12 knock-in accelerates these effects. Sox12 promotes HCC metastasis by increasing intratumoral regulatory T-cell (Treg) infiltration, decreasing CD8+ T-cell infiltration, and activating C-C motif chemokine ligand 22 (CCL22) and CD274 expression [1]. In multiple myeloma, Sox12 knockdown significantly reduces cell proliferation, colony formation, and upregulates apoptosis by down-regulating the Wnt/β-catenin signaling pathway [2]. In osteosarcoma, Sox12 knockdown inhibits spheroidization, expression of stemness markers, and tumor formation in nude mice [3]. In colorectal cancer, downregulation of Sox12 hampers cell proliferation and metastasis [5]. In thyroid cancer, Sox12 knockdown affects cell proliferation, migration, and invasion [6]. In esophageal squamous cell carcinoma, Sox12 knockdown inhibits colony forming efficiency, migration, and invasion of ESCC cells in vitro [7].

In conclusion, Sox12 plays important roles in multiple biological processes, especially in cancer development and progression. The use of KO and CKO mouse models has been instrumental in revealing its functions in specific disease areas such as HCC, multiple myeloma, osteosarcoma, colorectal cancer, thyroid cancer, and esophageal squamous cell carcinoma. These findings contribute to a better understanding of the molecular mechanisms underlying these diseases and may provide potential therapeutic targets.