LGALS1, also known as Galectin-1, is a glycan - binding protein. It regulates intracellular processes like signal transduction and extracellular ones such as immunity and leukocyte mobilization, supporting cell survival. It is well - known for its role in RAS signaling [2].

In glioblastoma, single - cell profiling and zebrafish xenograft models identified LGALS1 as a primary regulator of immunosuppression, with GBM - induced GAM polarization and related features correlating with patient survival [1]. In acute myeloid leukemia (AML), LGALS1 acts as a pro - survival molecule. Knockdown of LGALS1 in an in vivo murine OCI - AML3 xenograft model prolonged survival, and high LGALS1 mRNA in patients was associated with shorter disease - free survival [2]. In relapsed/refractory AML, chemotherapy - induced reprogramming led to upregulation of LGALS1 in quiescent stem - like cells involved in chemoresistance, and its inhibitor could enhance chemotherapy [4]. In intrahepatic cholangiocarcinoma, LGALS1+ fibroblasts promoted tumor cell proliferation and migration, and silencing LGALS1 in cancer - associated fibroblasts suppressed tumor formation in vivo [3].

In summary, LGALS1 plays crucial roles in multiple diseases, especially in cancer - related processes like immunosuppression, cell survival, and tumor cell proliferation and migration. Gene - knockout or knockdown models in various in vivo studies, such as murine xenograft models in AML, have been instrumental in revealing these functions, providing potential therapeutic targets for diseases like glioblastoma, AML, and intrahepatic cholangiocarcinoma.