VPS33B interacts with NESG1 to modulate EGFR/PI3K/AKT/c-Myc/P53/miR-133a-3p signaling and induce 5-fluorouracil sensitivity in nasopharyngeal carcinoma.
Profiling of somatic mutations and copy number variations (CNV) in NPC tumors identified alterations in RTK/RAS/PI3K, NOTCH, DNA repair, chromatin remodeling, cell cycle, NF-κB, and TGF-β pathways.
In conclusion, this integrative pharmacology-based analysis revealed the anti-NPC effects of RO might be related to its regulatory impact via the PI3K-AKT signaling pathway, the Wnt signaling pathway, and the cAMP signaling pathway by targeting VEGFA, TP53, and HSPA8.
Moreover, we explored whether HAGLROS modulated the expression of autophagy-related gene 14 (ATG14) by competitively sponging miR-100, and then regulated the briskness of PI3K/AKT/mTOR signals in NPC development.
miR-144-3p was significantly overexpressed, whereas PTEN was more underexpressed in tumor tissues than in adjacent tissues. miR-144-3p promoted the proliferation and invasion of NPC cells and inhibited apoptosis by directly targeting PTEN, which improves PI3K-Akt signaling. miR-144-3p forced epithelial-mesenchymal transition in NPC.
Taken together, our data suggest that APLNR could potentially predict prognosis for patients with NPC and inhibit proliferation, migration, invasion, and EMT in nasopharyngeal cancer cells.-Liu, Y., Liu, Q., Chen, S., Liu, Y., Huang, Y., Chen, P., Li, X., Gao, G., Xu, K., Fan, S., Zeng, Z., Xiong, W., Tan, M., Li, G., Zhang, W. APLNR is involved in ATRA-induced growth inhibition of nasopharyngeal carcinoma and may suppress EMT through PI3K-Akt-mTOR signaling.
Galangin effects on apoptosis and S-phase arrest in NPC cells are mediated via interfering with the PI3K-AKT signaling pathway in a p53-independent manner.
Downregulation of monocarboxylate transporter 1 inhibits the invasion and migration through suppression of the PI3K/Akt signaling pathway in human nasopharyngeal carcinoma cells.
In conclusion, TCS radiosensitized NPC <i>in vitro</i> and <i>in vivo</i> via downregulation of PI3K pathways and the upregulation of cleaved caspase-3.
In conclusion, these results indicate that camptothecin treatment may inhibit the viability of NPC cells and aggressiveness by regulating the TGF-β-induced PI3K/AKT signaling pathways, which in turn may be a potential molecular target for the treatment of NPC.
Pre-treatment with angiotensin-(1-7) inhibits tumor growth via autophagy by downregulating PI3K/Akt/mTOR signaling in human nasopharyngeal carcinoma xenografts.
These results reveal a novel mechanism by which miR-296-3p negatively regulated by nicotine directly targets MK2-induced Ras/Braf/Erk/Mek/c-Myc or PI3K/AKT/c-Myc signaling to stimulate its own expression and suppress NPC cell proliferation and metastasis. miR-296-3p may thus serve as a therapeutic target to reverse chemotherapy resistance of NPC.
Traditional Herbal Formula NPC01 Exerts Antiangiogenic Effects through Inhibiting the PI3K/Akt/mTOR Signaling Pathway in Nasopharyngeal Carcinoma Cells.
The expression of Klf4 in the nucleus can be used as a biomarker for predicting the effects of cetuximab treatment in nasopharyngeal carcinoma, which might be attributed to the H-RAS and PI3K mutations, leading to cetuximab resistance.
To investigate the effects of microRNA-122 (miR-122) on the proliferation and apoptosis of nasopharyngeal carcinoma (NPC) HONE-1 cells, and its correlation with the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway.