Fig. 6From: Hypoxia upregulating ACSS2 enhances lipid metabolism reprogramming through HMGCS1 mediated PI3K/AKT/mTOR pathway to promote the progression of pancreatic neuroendocrine neoplasmsHMGCS1 reversed the oncogenic effects of ACSS2 in vitro. A–D Overexpression of ACSS2 upregulated the expression of HMGCS1 and knockdown of ACSS2 downregulated the expression of HMGCS1 by qRT-PCR and WB. E Co-IP demonstrated ACSS2 and HMGCS1 interaction. F, G CCK-8 assay indicated that overexpression of HMGCS1 reversed the tumor-suppressive effect of ACSS2 knocked down. H, I The colony formation suggested that overexpression of HMGCS1 reversed the tumor-suppressive effect of ACSS2 knocked down. J, K EdU assay indicated that overexpression of HMGCS1 reversed the DNA synthesis suppressed effect of ACSS2 knocked down. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001Back to article page