Anln, also known as anillin, is a mitosis-related protein. It plays a crucial role in promoting contractile ring formation and cytokinesis, which are essential processes in cell division. Anln is involved in multiple signaling pathways, such as the PI3K/AKT, MAPK, and JNK pathways, and is of great biological importance in cancer development [1,4,6]. Genetic models, like gene knockout (KO) or conditional knockout (CKO) mouse models, can be valuable for studying its functions.

In various cancers, Anln shows oncogenic properties. In esophageal squamous cell carcinoma (ESCC), high Anln expression promotes cytokinesis and proliferation, and targeting the USP10-Anln axis can inhibit ESCC cell-cycle progression [1]. In hepatocellular carcinoma (HCC), the cholesterol-TAZ-TEAD2-Anln/KIF23 pathway drives HCC proliferation [2]. In lung adenocarcinoma, Anln is activated, and miR-30a-5p can restrain its malignant progression by targeting Anln [3]. Knockdown of Anln in lung adenocarcinoma inhibits cell progression via pyroptosis activation [8]. In colorectal carcinoma, Anln promotes cell proliferation through the PI3K/AKT and MAPK pathways [4]. In oral cancer, Anln contributes to cancer progression by regulating the PI3K/mTOR signaling pathway [5]. In bladder urothelial carcinoma, Anln acts as an oncogene by activating the JNK signal pathway [6]. In pancreatic cancer, Anln promotes cancer progression by mediating the EZH2/miR-218-5p/LASP1 signaling axis [7]. In triple-negative breast cancer, knockout of Anln inhibits spheroid growth and affects cancer stem cell-related genes like TWIST1 and BMP2 [9].

In conclusion, Anln is mainly involved in cell division-related biological functions, and its dysregulation is closely associated with the development and progression of multiple cancers. Studies using KO or CKO mouse models would further clarify its role in these disease conditions, potentially providing new therapeutic targets for cancer treatment.