In this study, the human liver cancer cell line HepG2 was pre-cultured in different oxygen environments to examine the possible mechanisms of hypoxia-induced doxorubicin resistance.
Mechanism study showed that veliparib could significantly enhance the accumulation of doxorubicin in ABCB1-overexpression liver cancer cells, without down-regulating the expression level of ABCB1.
Therefore, the cytotoxic effect of OA was evaluated on human breast cancer MDA-MB-231 and human liver cancer HepG2 with absence and presence of P-gp, respectively.
Hence, co-treatment with an ABCB1 inhibitor and an anticancer agent may be effective for the treatment of patients with liver cancer containing the C-terminal truncated HBx.[BMB Reports 2019; 52(5): 330-335].
These findings suggest that the knockdown of NANOG in HepG2 human cells resulted in decreased MDR1 expression and increased doxorubicin sensitivity, and NANOG could be used as a novel potential therapeutic target to reverse multidrug resistance of liver cancer.
Multidrug resistance (MDR) has become a major impediment to a successful treatment for liver cancer patients, and one of the common reasons for MDR is the activation of ABCB1 gene, leading to the over-expression of P-glycoprotein (P-gp), which conferred cancer cells be resistant to a broad range of anticancer drugs.
To explore whether P-glycoprotein (Pgp) and other pumps, multidrug resistance-associated protein (MRP) and lung resistance protein (LRP), could affect tumor accumulation and efflux of 99mTc-MIBI in liver cancer.