Dual Inhibition of PI3K/Akt/mTOR Signaling Pathway in Leukemic Cell Lines Upregulates Long Non-Coding RNAs RNCR3 UCA1 and HULC

Decades of comprehensive research have resulted in a better understanding the crucial role phosphatidylinositol-3-kinase/protein kinase B/mammalian target rapamycin signaling different types leukemia whereby it strongly influences growth and survival cancerous cells. Recently, small-molecule inhibitors been introduced as targeted therapies that are more tolerable than conventional antineoplastic drugs for leukemia. The inhibition assays were performed to assess effectiveness pathway like everolimus, torkinib phosphokinase inhibitor 402 cell lines. cycle profiles, protein B S6 phosphorylations assessed by flow cytometry. We also screened expression 96 cancer-associated long non-coding RNAs upon inhibition. Compared untreated cells, smallmolecule treated cells showed reduced viability. Phosphokinase 402, dual was most effective all lines (56.6 %, 32.5 % 11.4 Jurkat, HL-60 K562 respectively). In addition, treatment with this shift G1 phase from S1 (Jurkat, G1: 12.2 S1: 4.9 %; HL-60, 38.4 44.4 14.4 15.7 %), effectively everolimus or torkinib. It observed when used, retinal RNA 3 (3-fold) highly up-regulated liver cancer (2-fold) levels significantly elevated whereas antisense ribonucleic acid INK4 locus zinc finger homeobox 2 decreased at least 25 %. Our findings revealed dualspecificity potent single-specificity inhibitors. Hence, dual-targeted therapy may be promising therapeutic option play key drug resistance could potential novel target.