Specifically, targeting cellular pathways frequently altered in glioblastoma, such as the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR), the p53 and the retinoblastoma (RB) pathways, or epidermal growth factor receptor (EGFR) gene amplification or mutation, have failed to improve outcome, likely because of redundant compensatory mechanisms, insufficient target coverage related in part to the blood brain barrier, or poor tolerability and safety.
Overexpression of Biglycan is Associated with Resistance to Rapamycin in Human WERI-Rb-1 Retinoblastoma Cells by Inducing the Activation of the Phosphatidylinositol 3-Kinases (PI3K)/Akt/Nuclear Factor kappa B (NF-κB) Signaling Pathway.
This study provides evidences that RB progression was suppressed by overexpressed miR-129-5p via direct targeting of PAX6 through PI3K/AKT signaling pathway, which may provide a molecular basis for better treatment for RB.
The present study aimed to explore whether microRNA (miR)‑182 regulates cell viability, invasion and angiogenesis in RB via the phosphatidylinositol‑3‑OH kinase (PI3K)/protein kinase B (AKT) signaling pathway and by targeting cell adhesion molecule 2 (CADM2).
Anticancer Effects of Gingerol in Retinoblastoma Cancer Cells (RB355 Cell Line) Are Mediated via Apoptosis Induction, Cell Cycle Arrest and Upregulation of PI3K/Akt Signaling Pathway.
In conclusion, our current study provided sufficient evidence to demonstrate that miR‑758 inhibits the progression of RB by directly targeting PAX6 and regulating the PI3K/Akt pathway, thereby suggesting that this miRNA may be developed as a therapeutic target for treating patients with RB.
These results demonstrate that a combination of carboplatin and bevacizumab results in a greater antitumor effect in advanced human retinoblastoma <i>in vitro</i> and <i>in vivo</i> by inhibiting the PI3K/Akt and MAPK/ERK pathways.
The objectives of this study were to determine if the AKT pathway is activated in human retinoblastomas and the extent that anti-PI3K therapy induces apoptosis in retinoblastoma cells, alone or in combination with the DNA damaging drugs carboplatin and topotecan.
Furthermore, BDNF overexpression rescued the tumour‑suppressing effects on RB cells induced by miR‑382. miR‑382 inactivated the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signalling pathway in RB.
Mechanically, our data demonstrated that tumor-promoting role of N-cadherin in thyroid cancer was closely related to the activities of the MAPK/Erk, the phosphatidylinositol-3-kinase (PI3K)/Akt and p16/Rb signaling pathways in addition to affecting the EMT process.
Moreover, according to the results of the IGF-1 assays, suppression of PI3K/Akt was a prerequisite for SHH inhibition, illuminating its potential role in the treatment of RB.
Typical molecular changes in glioblastoma include mutations in genes regulating receptor tyrosine kinase (RTK)/rat sarcoma (RAS)/phosphoinositide 3-kinase (PI3K), p53, and retinoblastoma protein (RB) signaling.
PIK3R3, an isoform of class IA phosphoinositide 3-kinase (PI3K), specifically interacts with cell proliferation regulators, such as retinoblastoma and proliferation cell nuclear antigen, to promote cell proliferation.
Genome-wide analyses have identified four major signaling nodes that are most frequently altered in prostate cancer: i) the androgen receptor (AR); ii) the PI3K pathway; iii) the Ras/Raf/MEK/ERK pathway; and iv) the retinoblastoma protein (pRB) signaling pathway.
Previously, we have shown that p55PIK, an isoform of class I(A) phosphoinositide 3-kinase (PI3K), specifically interacts with important cell-cycle regulators, such as retinoblastoma (Rb), to promote cell-cycle progression.
Mechanistically, in addition to targeting Met, Triflorcas alters phosphorylation levels of the PI3K-Akt pathway, mediating oncogenic dependency to Met, in addition to Retinoblastoma and nucleophosmin/B23, resulting in altered cell cycle progression and mitotic failure.
This study was designed to analyze AKT1 mutations in retinoblastoma and gain insights into the role PI3K-AKT pathway plays in the development of this tumor.