A study published in Hepatology, Impact Factor 14 magazine entitled "Baicalein Targets GTPase-Mediated Auto to Eliminate Liver Tumor-Limited Stem Cell-Like Cells Resumption to mTORC1 Inhibitation" found that scientists from the University of Southern California found that scientists from the University of California BC inhibits the autophage induced by mTORC1 inhibitors, and SAR1B is a target in liver convulsions and liver cancer cells that are inhibited by mTORC1.
Drug resistance is a major problem in the treatment of liver cancer. Mammal rapamycin target(mTORC1) inhibitors have been tested for liver cancer treatment based on highly active mTOR in the malignant tumor.
However, poor clinical trials are likely due to their ability to raise CD133 and promote chemotherapy tolerance. CD133 + tumor initiation stem cell-like cells(TICs) isolated from mouse and human liver tumors have chemical resistance and a method to eliminate this resistance needs to be found.
In order to find a compound that can eliminate TICs resistance to mTORC1 inhibition and improve the effects of chemotherapy, the researchers identified baicalin(BC), which selectively sensitized TICs and human liver cancer(HCC) cell-based Huh7 cells. However, it is not sensitive to primary hepatocytes in mice and humans.
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Nanobeads, mass spectrometry, biochemical binding experiments, and three-dimensional computational model studies show that BC has the ability to competitively inhibit the binding of guanosine triphosphatase to SAR1B guanosine triphosphatase, which is essential for autophagy. In fact, BC inhibits the autophage induced by mTORC1 inhibitors and cooperates with TIC and Huh7 spherical formation and mTORC1 inhibits cell death in patient-derived liver cancer xenotransplantation models.
In cancer cells treated with mTORC1 inhibitors, the expression of SAR1B saved BC-induced chemical sensitization, and the expression of SAR1B inhibited chemical sensitization.