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Phospholipase C-related catalytically inactive protein (PRIP)-deficient mouse embryonic fibroblasts exhibited increased cell migration, and was significantly attenuated upon transfection with a siRNA targeting p110alpha, a catalytic subunit of class I phosphoinositide 3-kinases (PIK3CA).
Here, we demonstrated that inducible MuSC-specific deletion of p110alpha, a catalytic subunit of phosphatidylinositol 3-kinase (PI3K), rendered MuSCs unable to exit quiescence, resulting in severely impaired MuSC proliferation and muscle regeneration.
miR152 may have an important role in pancreatic beta cell function, and established an association between miR152 and the PI3Kalpha axis.
H1047R mutation of Pik3ca induces centrosome amplification in cultured mouse cells.
The crucial role of p110beta and the more subtle role of p110alpha in the production of PIP3 molecular species following platelet stimulation has been demonstrated.
Here, we describe a role for PI3K/AKT in the regulation of TRF1, an essential component of the shelterin complex. PI3K and AKT chemical inhibitors reduce TRF1 telomeric foci and lead to increased telomeric DNA damage and fragility. We identify the PI3Kalpha isoform as responsible for this TRF1 inhibition.
The data establish oncogenic PIK3CA mutations as a cause of glutamine dependency in colorectal cancer.
High PI3k expression is associated with gastrointestinal stromal tumor.
High PI3K expression is sensitive to initial injury intensity induced by freeze damage.
excessive proliferation of endometrial epithelial cells was observed in Pik3cad/d mice. Our studies suggest that Pik3ca has a critical role in uterine gland development and female fertility
Long latency DMBA induced mouse mammary tumors reproduce the molecular profile of human luminal breast carcinomas, displaying a high incidence of activating Pik3caH1047 and loss of function Pten mutations.
Data show that the phosphoinositide 3-kinase (PI3K) inhibitor BKM120 led to a precipitous drop in DNA synthesis within 8 h of drug treatment, whereas DNA synthesis in normal tissues was less affected.
Using genetic inactivation of the growth and metabolism regulator, Pik3ca (encoding PIK3CA also known as p110alpha, alpha/+), the interplay between the maternal genome and the fetal genome on placental phenotype, was examined.
these results identify the PI3K-GSK3-SMAD1 axis as a central node integrating multiple signaling networks that govern bone formation and homeostasis.
Data suggest a critical role for KDM3A in the PI3K/AP-1 oncogenic axis and propose a novel strategy for inhibition of KDM3A against liver tumor development under PI3K pathway activation.
Data show that tumors lacking PSMA had less than half the abundance of type 1 insulin-like growth factor receptor (IGF-1R), less activity in the survival pathway mediated by PI3K-AKT signaling, and more activity in the proliferative pathway mediated by MAPK-ERK1/2 signaling.
Both PIK3CA mutants H1047R and E545K are able to activate the AKT/mTOR pathway. An intact AKT2/mTOR complex 1 cascade is required for tumourigenesis induced by H1047R/c-Met or E545K/c-Met in the liver in mice.
Loss of HDAC-mediated repression and gain of NF-kappaB activation underlie cytokine induction in ARID1A- and PIK3CA-mutation-driven ovarian cancer.
We further demonstrate that loss of one allele of PTEN is sufficient to shift isoform dependency from p110alpha to p110beta in vivo. These results provide insight into the molecular mechanism by which ErbB2-positive breast cancer escapes p110alpha inhibition.
Studies indicate that the Pten+/- genotype displayed neoplasia in multiple organs, including the endometrium and that the Pten is a key regulatory player in the PI3K/PTEN/AKT pathway.
Targeting activating mutations in PIK3CA assay was used for screening tumor DNA from Metastatic Relapse in Advanced Bladder Cancer patients; at least one mutation was detected in 19 of the 60 patients.
Six mutations located at the BRAF, KRAS, and PIK3CA genes have been detected in colorectal cancer patients using a novel multiplex surface enhanced Raman spectroscopy-multiplex PCR method.
Inflammatory stress displayed by endothelial cells derived from lymphatic malformation is consistent with errors in lipid metabolism that may be linked to PIK3CA acquired mutations.
Results show that activating PIK3CA mutations in lymphatic malformations are specifically localized in lymphatic endothelial cells (LECs); identified a new mutation in exon 10 and a Glu109 deletion of the gene and show that several kinase inhibitors have the potential to block LEC proliferation.
Levels of miR381 were decreased in clear cell and endometrioid carcinoma ovarian cancer. Experimentally induced upregulation of miR381 led to a decrease in the level of PIK3CA in ovarian cancer cells and inhibition of ovarian cancer cells proliferation and migration.
High PIK3CA expression is associated with gastric cancer.
PIK3CA overexpression is associated with esophageal squamous cell cancer.
a subset of PIK3CAmut promote tumorigenesis
PIK3CA copy number aberration and activation of the PI3K-AKT-mTOR pathway in varied disease states of penile cancer
We identified a total of five distinct mutations in PIK3CA (NM_006218.2), including one hotspot mutation (c.1624G>A;p.Glu542Lys); two recurrent, strong (gain of function) mutations (c.3140A>T;p.His1047Leu, c.1258T>C;p.Cys420Arg); one previously described mutation in patients with macrodactyly (c.344G>C;p.Arg115Pro); and one novel somatic PIK3CA mutation (c.248T>C; p.Phe83Ser) not previously described
PIK3CA mutation in gastric cancer is a rare finding. It is strongly associated with the microsatellite instability (MSI) molecular subgroup, presenting a worse outcome than other MSI patients. A completely different outcome is associated with the mutation in exon 9 compared to the mutation in exon 20, with the latter being more favorable.
In early breast cancer, PIK3CA mutations seem to identify HER2+ patients who are less likely to reach pCR. The clinical implications of PIK3CA mutations tend to vary between exon 9 and exon 20. This mechanism should be explored in further studies.
The majority of PIK3CA H1047R mutations in the breast cancer cohort precede genome doubling.
in Stage I colorectal cancer presence of KRAS mutations, that of simultaneous mutations in PIK3CA gene, or that of multiple KRAS mutations was significantly associated with shorter cancer specific survival; PIK3CA or multiple KRAS mutations were associated with nodal micrometastases and poorly differentiated clusters G3 as well
CTNNB1 mutations were found in 60% of Basal cell adenoma but not in basal cell adenocarcinoma. None of the tested cases had PIK3CA mutations. CTNNB1 mutation trended to be more common in those cases having a predominant tubular or tubulotrabecular patterns.
High PI3K expression is associated with metastasis in ovarian cancer.
phenotypic changes in metabolism following a single copy knock-in of mutant PIK3CA (H1047R) in the MCF10A cell line, an important cell model for studying oncogenic transformation in breast tissues, were examined.
The PIK3CA and PIK3R1 impactful mutations exhibit a mutually exclusive pattern, leading to oncogenesis and hyperactivity of PI3K pathway in breast cancer.
Data show that both class I and III phosphoinositide 3-kinases (PI3Ks) re present in trafficking vesicles.
There are multiple conformations in equilibrium during the course of PI3K SH3 domain unfolding.
PI3K has a role in activation of 5'-AMP-activated kinase during hypoxia-reoxygenation of bovine aortic endothelial cells
Production of PtdIns3P by PI3K-C2alpha is required for acquisition of fusion competence in neurosecretion.
crystallographic and biochemical approaches used to gain insight into activating mutations in two noncatalytic p110alpha domains-the adaptor-binding and the helical domains
Phosphatidylinositol 3-kinase is composed of an 85 kDa regulatory subunit and a 110 kDa catalytic subunit. The protein encoded by this gene represents the catalytic subunit, which uses ATP to phosphorylate PtdIns, PtdIns4P and PtdIns(4,5)P2. This gene has been found to be oncogenic and has been implicated in cervical cancers.
phosphoinositide-3-kinase, catalytic, alpha polypeptide
, Phosphoinositide-3-kinase, catalytic, alpha polypeptide
, PI3-kinase subunit alpha
, phosphatidylinositol 4,5-bisphosphate 3-kinase 110 kDa catalytic subunit alpha
, phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit alpha isoform
, phosphatidylinositol-4,5-bisphosphate 3-kinase 110 kDa catalytic subunit alpha
, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha isoform
, phosphoinositide-3-kinase catalytic alpha polypeptide
, ptdIns-3-kinase subunit alpha
, ptdIns-3-kinase subunit p110-alpha
, serine/threonine protein kinase PIK3CA
, PI3-kinase p110 subunit alpha
, phosphatidylinositol 3-kinase, catalytic, 110-KD, alpha
, phosphatidylinositol 3-kinase, catalytic, alpha polypeptide
, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit, alpha isoform
, ptdIns-3-kinase p110
, phosphoinositide 3-kinase catalytic subunit