Overexpression of PSAT1 regulated by G9A sustains cell proliferation in colorectal cancer

作者：Huijuan Wang, Longzhen Cui, Dandan Li, Ming Fan, Zhangnan Liu, Chunqi Liu, Sijing Pan, Lei Zhang, Hailong Zhang, Yinglan Zhao · 发表于：Signal Transduction and Targeted Therapy · 年份：2020 · DOI：10.1038/s41392-020-0147-5 · 被引用次数：47 · 研究领域：Cancer, Hypoxia, and Metabolism、Amino Acid Enzymes and Metabolism、Genetic factors in colorectal cancer

Colorectal cancer (CRC) is one of the most common cancers that contributes to cancer morbidity and mortality according to the National Cancer Institute’s report. The standard of care is still surgical resection and neoadjuvant chemoradiation therapy, which may result in serious effects on quality of life in patients. 1 Currently, many efforts have been aimed at precision medicine in CRC, which highlights the urgent need to identify accurate biomarkers for diagnosis and treatment that can be translated into clinical use. 2 As an important precursor for biomolecule synthesis, serine plays an essential role in cell proliferation. Recently, the serine synthesis pathway (SSP) has been shown to be activated during the pathogenesis of many cancers. 3 Phosphoserine aminotransferase (PSAT1), the enzyme that catalyzes the second step of the SSP, has been shown to correlate with cell proliferation and cancer development. 4 Overexpression of PSAT1 was found in non-small cell lung cancer, breast cancer, and esophageal squamous cell carcinoma and was shown to enhance tumorigenesis and metastasis. 5 These studies suggested that PSAT1 could play a role as a proproliferative and prosurvival factor in the process of carcinogenesis. However, less is known about the expression of PSAT1 and the underlying mechanism in CRC, which prompted us to explore its role and regulatory mechanism in the initiation and development of CRC.