Published online Aug 15, 2023. doi: 10.4251/wjgo.v15.i8.1400
Peer-review started: April 26, 2023
First decision: June 15, 2023
Revised: June 16, 2023
Accepted: July 17, 2023
Article in press: July 17, 2023
Published online: August 15, 2023
Processing time: 106 Days and 6.3 Hours
Resistance to sorafenib has become a challenge in clinical treatment of hepatocellular carcinoma (HCC). Physcion is a common bioactive anthraquinone that has potential as an anticancer agent.
To study the effect of physcion on sensitizing HCC cells to sorafenib.
Sorafenib-resistant HCC cells were established and treated with sorafenib and/or physcion. The cell viability, proliferation and apoptosis were measured by cell counting kit-8, colony formation, flow cytometry, and in vivo xenograft model. Glucose uptake, lactate acid production, extracellular acidification rate (ECAR), and oxygen consumption rate (OCR) were measured to analyze glycolysis. Expression of glycolysis-related regulators was assessed by western blotting.
The addition of physcion significantly enhanced the antitumor effects of sorafenib on sorafenib-resistant HCC cells, manifested by enhanced apoptosis and suppre
Our data indicated that physcion enhanced the sensitivity of HCC cells to sorafenib by enhancing miR-370 to suppress PIM1-promoted glycolysis.
Core tip: This study investigated the effects of physcion on sorafenib resistance of hepatocellular carcinoma (HCC) cells. Through utilizing in vitro and in vivo models, we found that physcion significantly enhanced the antitumor effects of sorafenib on sorafenib-resistant HCC cells, inducing apoptosis and suppressing cell growth. Further exploration on the mechanisms identified that physcion repressed HCC cells glycolysis by targeting the miRNA-370/PIM1 axis, which consequently sensitized HCC cells to sorafenib.