Lin9 is a subunit of the DREAM complex, playing a crucial role in regulating cell mitotic processes, cell-cycle progression, and gene expression during the cell cycle [3,4]. It is associated with pathways related to cell proliferation, and its proper function is of great biological importance for embryonic development, cell survival, and maintaining genome stability [3,4,5]. Genetic models, such as gene-knockout (KO) models in mice and zebrafish, have been valuable for studying Lin9 [4,5].

In KO mouse models, loss of Lin9 abolishes cell proliferation and leads to multiple mitotic and cytokinesis defects due to down-regulation of a large set of mitotic genes like Plk1, Aurora A, and Kif20a, indicating its essential role in early embryonic development and adult mouse viability. Lin9-heterozygous mice are more susceptible to lung tumorigenesis induced by oncogenic c-Raf, suggesting it may function as a haploinsufficient tumor suppressor [4]. In zebrafish, Lin9-depleted embryonic cells accumulate in mitosis, followed by apoptosis, especially in the developing central nervous system, and a cohort of Lin9-regulated genes for different mitotic processes was identified [5].

In conclusion, Lin9 is essential for regulating mitosis, cell proliferation, and genome stability. Studies using KO mouse and zebrafish models have revealed its significance in embryonic development and tumor suppression. High Lin9 expression is also related to poor clinical outcomes and drug resistance in some cancers, such as triple-negative breast cancer and lung adenocarcinoma, highlighting its potential as a therapeutic target in cancer treatment [1,2,6].