Lysine Deprivation Induces AKT-AADAT Signaling and Overcomes EGFR-TKIs Resistance in -Mutant Non-Small Cell Lung Cancer Cells.

Epidermal growth factor receptor () mutations are the most common driver genes in non-small cell lung cancer (NSCLC), especially in the Asian population. Although EGFR-tyrosine kinase inhibitors (TKIs) are influential in the treatment of -mutant NSCLC patients, acquired resistance inevitably occurs. Therefore, there is an urgent need to develop strategies to overcome this resistance.

The Inhibition of Wnt Restrain KRAS-Driven Metastasis in Non-Small-Cell Lung Cancer.

The mutations have been an obstacle to identify therapeutic targets in cancer treatment. In this work, we clarified the distinct metastasis pattern of non-small-cell lung carcinoma (NSCLC) induced by KRAS/KRAS mutations and inhibited the KRAS mediated metastasis by Wnt inhibitor. First, we found that KRAS induced more aggressive phenotype in vitro and in vivo experiments.

Punicalagin induces apoptotic and autophagic cell death in human U87MG glioma cells.

Aim: To investigate the effects of punicalagin, a polyphenol isolated from Punica granatum, on human U87MG glioma cells in vitro.

Methods: The viability of human U87MG glioma cells was evaluated using MTT assay. Cell cycle was detected with flow cytometry analysis.

MEK inhibitors reverse resistance in epidermal growth factor receptor mutation lung cancer cells with acquired resistance to gefitinib.

Lung adenocarcinoma cells harboring epidermal growth factor receptor (EGFR) mutations are sensitive to EGFR tyrosine kinase inhibitors (TKIs), including gefitinib. Acquired resistance to EGFR-TKIs develops after prolonged treatments. The study was prompt to explore effective strategies against resistance to EGFR-TKIs.