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Fig. 8 | Journal of Translational Medicine

Fig. 8

From: Hypoxia upregulating ACSS2 enhances lipid metabolism reprogramming through HMGCS1 mediated PI3K/AKT/mTOR pathway to promote the progression of pancreatic neuroendocrine neoplasms

Fig. 8

HMGCS1 regulated lipid metabolism and reversed the oncogenic effects of ACSS2 in vivo. A Overexpression of HMGCS1 in ACSS2 knocked down pNENs cells increased the cholesterol. B Overexpression of HMGCS1 in ACSS2 knocked down pNENs cells reduced the free fatty acids. C–E Tumor weight and volume were smaller in the ACSS2 knocked down group and further larger in the overexpression of HMGCS1 of ACSS2 knocked down group, The average TIR of ACSS2-sh group was 63.78%. F Knockdown of ACSS2 and overexpression of HMGCS1 of ACSS2 Knocked down successfully, Knockdown of ACSS2 inhibited the expression of proliferative index Ki67, while overexpression of HMGCS1 promotes the expression of proliferative index Ki67. *p < 0.05,**p < 0.01, ***p < 0.001, ****p < 0.0001

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