Gene basic information

Cancerhepatic cancer,


Linc-VLDLR is significantly up-regulated in malignant hepatocytes. Exposure of HCC cells to diverse anticancer agents such as sorafenib, camptothecin, and doxorubicin increases linc-VLDLR expression in cells as well as extracellular vesicles (EV) released from these cells. Incubation with EVs reduces chemotherapy-induced cell death and also increases linc-VLDLR expression in recipient cells. RNAi-mediated knockdown of linc-VLDLR decreases cell viability and abrogates cell-cycle progression. Moreover, knockdown of linc-VLDLR reduces expression of ABCG2 (ATP-binding cassette, subfamily G member 2), whereas overexpression of this protein reduces the effects of linc-VLDLR knockdown on sorafenib-induced cell death (1).

Cancer related information

download as excel csv txt

LncRNA tissue cancer type expression level oncogene/suppress gene pathway binding gene/factor associated gene/factor proliferation apoptosis migration EMT invasion metastasis prognosis tag PMID
0 linc-VLDLR liver hepatic cancer up onco ABCG2+ + chemotherapy resistance 24874432


[1]. Takahashi K, Yan IK, Wood J, Haga H, Patel T (2014). Involvement of extracellular vesicle long noncoding RNA (linc-VLDLR) in tumor cell responses to chemotherapy. Mol Cancer Res 12(10): 1377-87. link pubmed

© Bioinformatics Group of XTBG