To investigate whether microRNA-19a can promote the proliferative and migratory abilities of non-small cell lung cancer (NSCLC) cells by target inhibition of PTEN (phosphatase and tensin homolog deleted from chromosome 10, PTEN) expression, thus leading to the development of NSCLC.
<b>Conclusion:</b> Taken together, we proved that miR-224 might play essential roles in cellular functions of nutrient-depleted A549 cells possibly through regulating the target PTEN and downstream signal PI3K, suggesting the potential of miR-224 to be a therapeutic target for NSCLC therapy.
The present findings suggested that treatment with pemetrexed may exhibit synergistic effects with PTEN on lung cancer cells via the inhibition of the PI3K/AKT/mTOR signaling pathway and through carbohydrate metabolism, and treatment with pemetrexed combined with PTEN overexpression may represent a novel therapeutic strategy for the treatment of NSCLC.
We have conducted this study to check the effect of VCN-2 on the cell viability and the effect on PTEN (Phosphatase and tensin homolog), PI3KCA (Phosphatidylinositol 4, 5-biphosphate 3-kinase catalytic subunit alpha isoform/PI3K 110α subunit), and Akt1 when VCN-2 was used alone and in combination with radiation in the NSCLC cell line NCI-H23 (H23).
We firstly indicated that miR-4299 may be a candidate independent marker for NSCLC prognosis and suppressed the progression of NSCLC by modulating the activation of PTEN/AKT/PI3K signaling pathway, suggesting that miR-4299 could be a potential target for developing therapies in treating NSCLC.
In this study, we showed that YM155 markedly enhanced the sensitivity of erlotinib to EGFR-TKI resistant NSCLC cell lines H1650 (EGFR exon 19 deletion and PTEN loss) and A549 (EGFR wild type and KRAS mutation) through inducing autophagy-dependent apoptosis and autophagic cell death.
In order to further investigate the possible role of hsa_circ_0033155 in NSCLC progression, circRNA was overexpressed in NSCLC cells and it was observed that the overexpression of hsa_circ_0033155 significantly decreased cell proliferation, colony formation and migration, and elevated the level of phosphatase and tensin homolog deleted on chromosome 10, a tumor suppressor in many types of tumor.
In total 50 plasma samples from patients newly diagnosed with advanced NSCLC or resistant to first-line tyrosine kinase inhibitors (TKIs) were subjected to deep sequencing on a seven-gene panel (BRAF, EGFR, ERBB2, KRAS, NRAS, PIK3CA, PTEN) incorporated with molecular barcodes to improve accuracy in variant detection.
To the best of our knowledge, this is the first case of NSCLC harboring concurrent PTEN and TP53 mutations with widespread and strong coexpression of TTF-1 and p40, which has been confirmed in the resected specimen, and only the second documented case of NSCLC with TTF-1 and p40 diffuse coexpression in the carcinoma cells from the same individual.