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ANGPTL3 overcomes sorafenib resistance via suppression of SNAI1 and CPT1A in liver cancer.
Transl Oncol
December 2024
Liver Research Center, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan; Institute of Stem Cell and Translational Cancer Research, Chang Gung Memorial Hospital, Linkou, Taoyuan, Taiwan. Electronic address:
Liver cancer, encompassing hepatocellular carcinoma (HCC) and hepatoblastoma, the latter of which primarily occurs in early childhood, is the most common malignant tumor arising from liver and is responsible for a significant number of cancer-related deaths worldwide. Targeted drugs have been used for anti-liver cancer treatment in the advanced stage, while their efficacy is greatly compromised by development of drug resistance. Drug resistance is a complicated process regulated by intrinsic and extrinsic signals and has been associated with poorer prognosis in cancer patients.
View Article and Find Full Text PDF5-methylcytosine methylation of MALAT1 promotes resistance to sorafenib in hepatocellular carcinoma through ELAVL1/SLC7A11-mediated ferroptosis.
Drug Resist Updat
January 2025
Cancer Center, Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen, Guangdong 518000, PR China; Shenzhen Traditional Chinese Medicine Oncology Medical Center, Shenzhen, Guangdong 518000, PR China. Electronic address:
Emerging evidence demonstrates that long non-coding RNAs (lncRNAs) play a crucial role in sorafenib resistance in hepatocellular carcinoma (HCC), and lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a dysregulated lncRNA in sorafenib-resistant HCC cells. However, the underlying regulatory mechanisms of MALAT1 in sorafenib-resistant HCC cells remain unclear. In the present study, we demonstrated that 5-methylcytosine (mC) methylation catalyzed by NSUN2 and ALYREF contributed to the RNA stability and upregulation of MALAT1.
View Article and Find Full Text PDFRegulatory factor X1 promotes sorafenib-induced ferroptosis in hepatocellular carcinoma by transcriptional regulation of BECN1.
Cell Oncol (Dordr)
December 2024
State Key Laboratory of Oncology in South China and Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Article Synopsis
- Sorafenib is a first-line drug for advanced hepatocellular carcinoma (HCC), which shows limited effectiveness, but may induce cell death through a process called ferroptosis.
- The study identified a key regulatory factor, RFX1, that enhances ferroptosis in HCC cells by inhibiting a specific antiporter system and regulating the expression of the BECN1 gene.
- Findings suggest a new signaling loop involving STAT3 that promotes RFX1 expression and helps explain how sorafenib leads to HCC cell death, offering insights for potential therapeutic strategies.
Decreased lncRNA HNF4A-AS1 facilitates resistance to sorafenib-induced ferroptosis of hepatocellular carcinoma by reprogramming lipid metabolism.
Theranostics
December 2024
Department of Emergency Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Resistance to sorafenib remains a major challenge in the systemic therapy of liver cancer. However, the involvement of lipid metabolism-related lncRNAs in this process remains unclear. Different expression levels of lipid metabolism-related lncRNAs in HCC were compared by analysis of Gene Expression Omnibus and The Cancer Genome Atlas databases.
View Article and Find Full Text PDFSorafenib-induced macrophage extracellular traps via ARHGDIG/IL4/PADI4 axis confer drug resistance through inhibiting ferroptosis in hepatocellular carcinoma.
Biol Direct
November 2024
Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, People's Republic of China.
Background: Hepatocellular carcinoma (HCC) is one of the most common as well as leading causes of mortality worldwide, and sorafenib is the first-line treatment in HCC patients. Unfortunately, drug resistance to sorafenib often develops. However, the underlying mechanism remains unclear.
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