Abstract
Hepatocellular carcinoma (HCC) is the most common primary malignant tumor of the liver. Although progress has been made in diagnosis and treatment, morbidity and mortality continue to rise. Chronic liver disease and liver cirrhosis are still the most important risk factors for liver cancer. Although there are many treatments, it can only be cured by orthotopic liver transplantation (OLT) or surgical resection. And the worse the degree of differentiation, the worse the prognosis of patients with liver cancer. Then it can be considered that restoring a better state of differentiation may improve the prognosis. The differentiation treatment of liver cancer is to reverse the dedifferentiation process of hepatocytes to liver cancer cells by means of drugs, improve the differentiation state of the tumor, and restore the normal liver characteristics, so as to improve the prognosis. Understanding the mechanism of dedifferentiation of liver cancer can provide ideas for drug design. Liver enrichment of transcription factors, imbalance of signal pathway and changes of tumor microenvironment can promote the occurrence and development of liver cancer, and restoring its normal level can inhibit the malignant behavior of tumor. At present, some drugs have been proved to be effective, but more clinical data are needed to support the effectiveness and reliability of drugs. The differentiation treatment of liver cancer is expected to become an important part of the treatment of liver cancer in the future.
Highlights
Liver cancer is the sixth most common cancer disease globally, and the fourth leading cause of cancer death [1]
The expression of a-SMA can promote the expression of connective tissue growth factor (CTGF), and CTGF-mediated tumor-matrix interaction between hepatocellular carcinoma cells and hepatic stellate cells can promote the progression of Hepatocellular carcinoma (HCC) [47]
IL-34 mediates the interaction between tumor cells and Tumor-associated macrophage (TAM) [61]. especially in hepatocellular carcinoma, tumor cell-derived IL-34 can stimulate TAM to produce transforming growth factor b 1 (TGF-b 1), inhibit the expression of miR-28-5p on HCC cells [61], promote
Summary
Liver cancer is the sixth most common cancer disease globally, and the fourth leading cause of cancer death [1]. The high expression of HNF1b enhances the tumor-forming ability of HCC cells in vivo, and promotes the dedifferentiation of hepatocellular carcinoma cells into liver cancer stem cells by activating Notch signal pathway, as well as the invasion of HCC cells and the occurrence of EMT [11]. The expression of a-SMA (a marker of HSC activation) can promote the expression of connective tissue growth factor (CTGF), and CTGF-mediated tumor-matrix interaction between hepatocellular carcinoma cells and hepatic stellate cells can promote the progression of HCC [47]. Especially in hepatocellular carcinoma, tumor cell-derived IL-34 can stimulate TAM to produce transforming growth factor b 1 (TGF-b 1), inhibit the expression of miR-28-5p on HCC cells [61], promote IL-34 mediates the interaction between tumor cells and TAM [61]. especially in hepatocellular carcinoma, tumor cell-derived IL-34 can stimulate TAM to produce transforming growth factor b 1 (TGF-b 1), inhibit the expression of miR-28-5p on HCC cells [61], promote
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
