Cenpl, or Centromere protein L, is an important member of the centromere protein (CENP) family. It is involved in the mitotic process of eukaryotic cells, playing a crucial role in cell division. The gene is associated with multiple biological pathways, and its abnormal expression can have significant impacts on cell function and organism health [1,4].

Cenpl has been extensively studied in the context of cancer. In most cancers, Cenpl is up-regulated, and its overexpression and mutation are linked to a poorer prognosis [1]. For example, in lung adenocarcinoma (LUAD), Cenpl regulates cell proliferation and the cell cycle, and is negatively correlated with the inflammation level. Knockdown of Cenpl significantly suppresses the expression of CDK2 and CCNE2, and induces G0/G1 arrest and apoptosis of LUAD cells [1]. In breast cancer, high Cenpl expression is related to the cell cycle, nuclear division, organelle fission, and chromosome segregation. Knockdown of Cenpl decreases breast cancer cells' ability to proliferate and migrate [3]. In hepatocellular carcinoma (HCC), Cenpl is significantly up-regulated, and it accelerates cell proliferation, cell cycle, apoptosis, and glycolysis via the MEK1/2-ERK1/2 pathway [4]. In pancreatic adenocarcinoma, overexpression of Cenpl mRNA is significantly correlated with the poor prognosis of patients [2].

In conclusion, Cenpl is essential for the normal mitotic process in eukaryotic cells. Research using gene-knockdown models in cancer cells has revealed its significant role in cancer development, including promoting cell proliferation, influencing the cell cycle, and being associated with poor prognosis in multiple cancer types. These findings suggest that Cenpl could potentially serve as a biomarker and therapeutic target in cancer treatment.