Area of research
Orthopedics and Sports Medicine · Epidemiology
Research interest
Research focused on Sorafenib and Protein kinase B, with related work in Autophagy, Hepatocellular carcinoma, Cancer research. Notable publications include 'Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma', 'MiR-21 mediates sorafenib resistance of hepatocellular carcinoma cells by inhibiting autophagy via the PTEN/Akt pathway', and 'LncRNA SNHG1 contributes to sorafenib resistance by activating the Akt pathway and is positively regulated by miR-21 in hepatocellular carcinoma cells'.
Role of ITGB2 protein structure and molecular mechanism in precancerous lesions of gastric cancer: Influencing the occurrence and development of cancer through the CXCL1-CXCR2 axis
Correction to: LncRNA SNHG1 contributes to sorafenib resistance by activating the Akt pathway and is positively regulated by miR-21 in hepatocellular carcinoma cells
LncRNA SNHG1 contributes to sorafenib resistance by activating the Akt pathway and is positively regulated by miR-21 in hepatocellular carcinoma cells
MicroRNA-21-Regulated Activation of the Akt Pathway Participates in the Protective Effects of H<sub>2</sub>S against Liver Ischemia–Reperfusion Injury
An artificial lncRNA targeting multiple miRNAs overcomes sorafenib resistance in hepatocellular carcinoma cells
MiR-21 mediates sorafenib resistance of hepatocellular carcinoma cells by inhibiting autophagy via the PTEN/Akt pathway
Inhibition of Akt Reverses the Acquired Resistance to Sorafenib by Switching Protective Autophagy to Autophagic Cell Death in Hepatocellular Carcinoma
Enhanced Autophagy by Everolimus Contributes to the Antirestenotic Mechanisms in Vascular Smooth Muscle Cells
Spreading-vanishing dichotomy in a degenerate logistic model with general logistic nonlinear term
Up‐regulation of survivin by <scp>AKT</scp> and hypoxia‐inducible factor 1α contributes to cisplatin resistance in gastric cancer
Daidzein Induced Apoptosis via Down-Regulation of Bcl-2/Bax and Triggering of the Mitochondrial Pathway in BGC-823 Cells