Here we discuss our current understanding of the molecular events controlling cellular metabolism downstream of PI3K and AKT and of how these events couple two major hallmarks of cancer: growth factor independence through oncogenic signalling and metabolic reprogramming to support cell survival and proliferation.
Herein, in silico structure- and ligand-based approaches have been applied to screen in-house IIIM natural product repository for Akt1 (serine/threonine protein kinases) which is a well-known therapeutic target for cancer due to its overexpression and preventing the cells from undergoing apoptosis.
Frequent mutation of PI3K/AKT/mTOR signaling pathway genes in human cancers has stimulated large investments in targeted drugs but clinical successes are rare.
ACLY plays a pivotal role in cancer metabolism through the potential deprivation of cytosolic citrate, a process promoting glycolysis through the enhancement of the activities of PFK 1 and 2 with concomitant activation of oncogenic drivers such as PI3K/AKT which activate ACLY and the Warburg effect in a feed-back loop.
Here we provide a comprehensive review of the current knowledge on SOX2 protein modifications, their proposed relationship to the PI3K/AKT pathway, and regulatory influence on SOX2 with regards to stemness, reprogramming, and cancer.
The serine-threonine kinase AKT/PKB is a critical regulator of various essential cellular processes, and dysregulation of AKT has been implicated in many diseases, including cancer.
Receptor tyrosine kinases upstream of PI3K, the p110a catalytic fractional unit of PI3K, the downstream kinase, AKT, and therefore the negative regulator, PTEN, are all often altered in cancer.
PD-1 activity within malignant T cells can negatively regulate the PI3K/AKT and PKCθ/NF-κB tumor survival pathways and PD-1 is frequently inactivated in this human malignancy.
Among the relevant biological pathways, phosphatidylinositol 3-kinase/AKT (PIK3/AKT)-mammalian target of rapamycin (mTOR) signaling is frequently upregulated in this cancer.
Chronic <i>Helicobacter pylori</i> infection increases the risk of gastric cancer and induction of hypoxia-induced factor (HIF), which is frequently associated with the development and progression of several types of cancer.We recently showed that <i>H. pylori</i> activation of the PI3K-AKT-mTOR pathway in gastric cells increased HIF-1α expression.Here, we identified the <i>H. pylori</i> virulence factor responsible for HIF-1α induction.A mutant of the <i>H. pylori</i> 84-183 strain was identified with reduced ability to induce HIF-1α.
K-Ras<sup>G12V/Y40C</sup>-PI3K/AKT pathway regulates H1.4<sup>S35ph</sup> through PKA to promote the occurrence and development of osteosarcoma cancer.
Although <i>PIK3CA</i> amplification associates with some surrogate measures of increased PI3K activity, markers for AKT1-3 and MTOR signaling are decreased, suggesting that this signaling is not a predominant pathway to promote cancer growth of aggressive serous-like UCEC.
We concluded that MAPK4 can promote cancer by activating the AKT/mTOR signaling pathway and that targeting MAPK4 may provide a novel therapeutic approach for cancer.
<b>K1</b> serves to downregulate various cancer survival signaling pathways (AKT, p38, IL-6, VEGF, and TNF-α) and upregulate an anti-inflammatory response (IL-10).
Studies in mammals indicate a role for VEPH1 in modulating TGFβ signaling and AKT activation, while numerous studies indicate VEPH1 expression is altered in several pathological conditions, including cancer.
These results elucidate that the inhibition of NF-ҡ B and PI3K/AKT is one of the most important mechanism by which BCP suppresses cancer cell proliferation and enhances apoptosis.
Molecular genetic aberrations in the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway are common in human cancers including glioblastoma, yet, novel therapeutic approaches targeting this pathway in glioblastoma have not been successful.