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
Hepatocellular carcinoma (HCC) is one of the most malignant cancer types with high morbidity and mortality. Currently, patients with advanced HCC usually receive systemic local treatment with ablation or external irradiation along with sorafenib. Resistance to sorafenib has become a challenge in clinical treatment of HCC.
Physcion is a common bioactive anthraquinone that is a potential anticancer agent that has been reported to regulate multiple intracellular signaling pathways via targeting protein kinases, cell cycle, transcriptional factors, miRNAs, and apoptosis-related proteins. The excessive glycolysis of cancer cells compared with normal cells, named as Warburg effect, is a major characteristic of cancer and play a critical role in cancer initiation and development.
This work aimed to study the effect of physcion on glycolysis metabolism and sensitizing the 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 assay.
The addition of physcion significantly enhanced the antitumor effects of sorafenib on sorafenib-resistant HCC cells, manifested by enhanced apoptosis and suppressed cell growth. The glucose uptake, lactate acid production, and ECAR were elevated, and OCR was suppressed under physcion treatment. The level of PIM1 was elevated and miR-370 was suppressed in sorafenib-resistant HCC cells compared with the parental cells, which was suppressed by physcion treatment. Inhibition of miR-370 notably reversed the effects of physcion on sorafenib-resistant HCC cells.
Physcion enhanced the sensitivity of HCC cells to sorafenib via enhancing miR-370 to suppress PIM1-promoted glycolysis.
As a potential anticancer agent, physcion possibly enhances sensitivity in other therapy resistance. Based on the multiple cellular processes that are regulated by physcion, it is possible that PIM1-regulated glycolysis may not be the only mechanism underlying sorafenib sensitivity. Further studies such as high-throughput sequencing analysis may be conducted to explore the comprehensive and in-depth effects of physcion in cancer.