https://www.selleckchem.com/products/gyy4137.html could significantly increase the expression of cleaved caspase-3, Bax, E-cadherin and GSK-3β but reduce the expression of Bcl-2, N-cadherin, vimentin, Wnt1 and β-catenin in MHCC97H and HCCLM3 cells. In addition, Wnt/β-catenin pathway inhibitor (IWP-2) partially reversed the effects of silencing on the proliferation, migration, invasion and apoptosis of HCCLM3 cells. Our study demonstrated that can suppress cell proliferation, migration and invasion, as well as promote apoptosis of HCC cells via modulation of the Wnt/β-catenin signaling pathway. Our study demonstrated that ANCR can suppress cell proliferation, migration and invasion, as well as promote apoptosis of HCC cells via modulation of the Wnt/β-catenin signaling pathway.Several studies have shown that STK11 and TP53 mutations have different effects on the susceptibility to immune checkpoint blockade in KRAS-mutant non-small cell lung cancer (NSCLC). However, the impact of STK11/TP53 co-mutations on treatment outcomes in the same clinical setting has never been reported. We recently encountered a case of a 70-year-old man who was diagnosed with advanced lung adenocarcinoma with high-programmed death-ligand 1 (PD-L1) expression. He received pembrolizumab monotherapy as a frontline treatment; however, the tumor did not respond to this therapy and showed deleterious outcome. Next-generation sequencing revealed that the tumor harbored a rare STK11/TP53/KRAS triple mutation. Our case suggests that these compound mutations may constitute a distinct, aggressive subset that is resistant to immunotherapy even when the tumor strongly expresses PD-L1. In addition, this report highlights the importance of using molecular profiling to detect co-mutations that can be associated with primary resistance or disease progression to improve survival even in the immunotherapy setting. Tyrosine kinase with immunoglobulin and epidermal growth factor homology domains 2 (Tie2)-expressi