Nanoparticles Loaded with GSK1059615 Combined with Sorafenib Inhibited Programmed Cell Death 1 Ligand 1 Expression by Negatively Regulating the PI3K/Akt/NF-KB Pathway, Thereby Reversing the Drug Resistance of Hepatocellular Carcinoma to Sorafenib

Activation of the cellular signaling pathways can induce sorafenib-resistant hepatocellular carcinoma (HCCR). In this work, the PI3K/mTOR inhibitor GSK1059615 inhibited the proliferation and invasion of HCCR cells. PLGA-PEG-mal diblock copolymer was used to load GSK1059615 and sorafenib, and the vector was further modified with GPC3 antibody IP: 1498 160 66 On: Wed, 22 Jun 2022 06:30:00 (hGC33) to obtain hGC33-modified GSK1059615 and soafeib-loaded nanoparticle(Ab-G/S-NP). Ab-G/S-NP regulated Copyright: American Scientific Publishers the activation of cellular signaling pathways in HCCR cells inhibiting the expression and activation of NF-???B and Delivered by Ingenta downregulating the level of programmed cell death 1 ligand 1(PD-L1) to reverse drug resistance of HCCR cells to sorafenib. These findings deserve further study in the combined treatment of HCCR cells with GSK1059615 in vivo to develop a more effective treatment of sorafenib-resistant cancers.

Automated summary

This study found that GSK1059615 inhibited the proliferation and invasion of sorafenib-resistant hepatocellular carcinoma cells. By modifying nanoparticles, the drug resistance of the cells to sorafenib was reversed. These findings are important for the development of more effective treatments for resistant cancers.