Smagp, short for Small trans-Membrane And Glycosylated Protein, is a novel small trans-membrane glycoprotein. It contains a trans-membrane domain and binding domains for protein 4.1 and the PDZ domain of MAGUK proteins, potentially being involved in a scaffolding protein complex, thus participating in epithelium organization or subsequent functions [4].

In multiple cancers, Smagp shows significant associations. In triple-negative breast cancer (TNBC), its up-regulation is linked to poorer overall survival, and loss of Smagp enhances the sensitivity of TNBC cells to doxorubicin treatment by regulating mitochondrial respiration [1]. In glioblastoma (GBM), silencing Smagp inhibits cell viability, colony formation, invasion, and promotes apoptosis by inactivating the PI3K/Akt pathway [2]. In cervical cancer, silencing Smagp induces cell cycle arrest, inhibits cell proliferation, colony formation, and suppresses tumorigenic potential in nude mice [3]. Overexpression of Smagp in a non-metastasizing rat pancreatic adenocarcinoma subline promotes metastasis formation [5].

In conclusion, Smagp is involved in the regulation of cancer-related processes such as chemotherapy sensitivity, cell proliferation, apoptosis, and metastasis. Gene knockout or knockdown models in these cancer types have revealed its role in specific biological processes, highlighting its potential as a therapeutic target for improving cancer treatment.