期刊论文

Cao, Deliang;Jin, Junfei

英文

Molecular Carcinogenesis

0899-1987

2018

57

10

1300-1310

10.1002/mc.22844

National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81472465, 81772842]; Natural Science Foundation of GuangxiNational Natural Science Foundation of Guangxi Province [2015GXNSFEA139003]; NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASESUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK) [P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579, P30DK020579] Funding Source: NIH RePORTER

本校为其他机构

Aldo-keto reductase 1B10 (AKR1B10) is upregulated in breast cancer and promotes tumor growth and metastasis. However, little is known of the molecular mechanisms of action. Herein we report that AKR1B10 activates lipid second messengers to stimulate cell proliferation. Our data showed that ectopic expression of AKR1B10 in breast cancer cells MCF-7 promoted lipogenesis and enhanced levels of lipid second messengers, including phosphatidylinositol bisphosphate (PIP2), diacylglycerol (DAG) and inositol triphosphate (IP3). In contrast, silencing of AKR1B10 in breast cancer cells BT-20 and colon ca...