Srsf9, or Serine/arginine-rich splicing factor 9, is a classical RNA-binding protein essential for regulating gene expression programs [2]. It functions in processes such as alternative splicing, which is a crucial post-transcriptional regulatory mechanism [4]. It is involved in multiple biological pathways, and its dysregulation is associated with various diseases, highlighting its overall biological importance. Genetic models, especially KO/CKO mouse models, can be valuable for studying its functions in vivo.

In cardiac hypertrophy, Mettl1-catalyzed m7G modification of Srsf9 mRNA increases Srsf9 expression, facilitating alternative splicing and stabilization of NFATc4, promoting cardiac hypertrophy. Knockdown of Srsf9 protects against TAC-or Mettl1-induced cardiac hypertrophic phenotypes in vivo and in vitro [1].

In colorectal cancer, Srsf9 promotes cancer progression by stabilizing DSN1 mRNA in an m6A-related manner, and knockdown of Srsf9 inhibits cell proliferation, migration, and invasion [2].

In glioblastoma, Srsf9 promotes cell proliferation and migration by enhancing CDK1 expression, and its elevated expression correlates with GBM stages and poor survival [3].

In oral cancer, Srsf9 mediates oncogenic RNA splicing of SLC37A4 via liquid-liquid phase separation to promote cancer progression, and disruption of Srsf9 LLPS prevents its regulatory influence on SLC37A4 splicing [5].

In ovarian cancer, a positive feedback loop of Srsf9/USP22/ZEB1 promotes cancer progression, and knockdown of Srsf9 suppresses the malignant phenotypes of OC cells [6].

In conclusion, Srsf9 is a key regulator in multiple biological processes. Model-based research, especially using KO/CKO mouse models, has revealed its role in diseases such as cardiac hypertrophy, colorectal cancer, glioblastoma, oral cancer, and ovarian cancer. Understanding Srsf9's functions provides potential therapeutic targets for these diseases.