SAA1 knockdown promotes the apoptosis of glioblastoma cells via downregulation of AKT signaling

In this study, we validate that SAA1 is up-regulated in GBM, and its high expression predicts poor prognosis. SAA1 knockdown promotes the apoptosis of GBM cell. Mechanistically, SAA1 knockdown can inhibit serine/threonine protein kinase B (AKT) phosphorylation, thereby regulating the expression of apoptosis-related proteins such as Bcl2 and Bax, leading to GBM cell death. Moreover, Gliomas with low SAA1 expression have increased sensitivity to Temozolomide (TMZ). Low SAA1 expression segregated glioma patients who were treated with Temozolomide (TMZ) or with high MGMT promoter methylation into survival groups in TCGA and CGGA dataset. Our study strongly suggested that SAA1 was a regulator of cells apoptosis and acted not only as a prognostic marker but also a novel biomarker of sensitivity of glioma to TMZ.

Source: Journal of Cancer - April 19, 2021 Category: Cancer & Oncology Authors: Huikai Zhang, Yang Xu, Gang Deng, Fanen Yuan, Yinqiu Tan, Lun Gao, Qian Sun, Yangzhi Qi, Kun Yang, Rongxin Geng, Hongxiang Jiang, Baohui Liu, Qianxue Chen Tags: Research Paper Source Type: research