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PIK3CA and p53 mutations promote 4NQO-initated head and neck tumor progression and metastasis in mice

ABSTRACT: The effect of gain of function mutations in p53, pik3ca, and both genes in mouse tongue subject to 4NQO treatment on gene expression is characterized by RNASeq.

ORGANISM(S): Mus musculus

PROVIDER: GSE143716 | GEO | 2022/04/19

REPOSITORIES: GEO

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PIK3CA and p53 mutations promote 4NQO-initated head and neck tumor progression and metastasis in mice

Project description:PIK3CA and p53 mutations promote 4NQO-initated head and neck tumor progression and metastasis in mice

| PRJNA601436 | ENA

<i>PIK3CA</i> and <i>p53</i> Mutations Promote 4NQO-Initated Head and Neck Tumor Progression and Metastasis in Mice.

Project description: Not available

| S-EPMC7272268 | biostudies-literature

Tongue tissue gene profile in 4NQO induced tongue carcinogenesis before and after IL-1Ra interference

Project description:Nine groups of rat tongue tissue RNA samples, including three from normal control, three from 4NQO induced tongue tissue, and three from 4NQO induced and IL-1Ra interference tongue tissue (3 rats per group) were collected for gene microarray hybridization.

2017-02-11 | GSE42855 | GEO

4NQO treatment may modulate gene expression in mouse tongue

Project description:Determine whether 4NQO treatment may modulate gene expression in mouse tongue. C57BL/6J mice were given 4NQO (100ug/ml in drink) for 8 weeks; Non-treated control samples were used for comparison.

2016-05-24 | GSE75374 | GEO

A head and neck cancer protein interaction map reveals PIK3CA mutant drug sensitivity

Project description:Despite extensive DNA sequencing of patient tumors, it remains challenging to translate the immense landscape of heterogeneous genetic alterations into function and clinical outcomes due to a limited understanding of cancer specific molecular network architectures. To bridge this gap, we have used affinity purification-mass spectrometry to generate protein interaction networks for 31 proteins with significant alterations in head and neck squamous cell carcinoma. This network includes 771 interactions covering both cancer and non-tumorigenic cell states, as well as wild-type and mutant proteins. Differential analysis across these dimensions reveals a strong interaction between PIK3CA and ERBB3 (HER3), dependent upon mutations in PIK3CA. We show that this interaction correlates with ERBB3 activity in vitro and can be targeted in vivo using a clinical ERBB3 inhibitor, CDX3379, to prohibit growth of tumors with common PIK3CA mutations. This study provides a roadmap for elucidating genetic complexity through multidimensional maps of cancer cell biology.

2021-10-07 | PXD019469 | Pride

PIK3CA mutations in head and neck squamous cell carcinoma.

Project description: Not available

| S-EPMC1780023 | biostudies-other

Overexpression of PIK3CA in head and neck squamous cell carcinoma is associated with poor outcome and activation of the YAP pathway

Project description:Objectives: Phosphatidylinositol 3-kinase catalytic subunit alpha (PIK3CA) is commonly altered in many human tumors, leading to the activation of p110α enzymatic activity that stimulates growth factor-independent cell growth. PIK3CA alterations such as mutation, gene amplification and overexpression are common in head and neck squamous cell carcinoma (HNSCC) and. We aim to explore how these alterations and clinical outcome are associated, as well as the molecular mechanisms involved. Material and methods: Mutation and copy-number variation in PIK3CA, and whole-genome expression profiles, were analyzed in primary HNSCC tumors from The Cancer Genome Atlas (TCGA) cohort (n=243). The results were validated in an independent cohort form the University Hospital of A Coruña (UHAC, n=62). Expression of the PIK3CA gene protein product (PI3K p110α) and nuclear YAP were assessed in tissue microarrays in a cohort from the University Hospital 12 de Octubre (UH12O, n=91). Results: Only high expression of the PIK3CA gene was associated with poor clinical outcome. The study of gene expression, transcription factor and protein signatures suggested that the activation of the Hippo-YAP pathway, involved in organ size, stem cell maintenance and tumorigenesis, could underlie tumor progression in PI3KCA overexpressing tumors. Tissue arrays showed that PI3K p110α levels correlated with YAP nuclear localization in HNSCC tumors. Conclusions: High expression of PIK3CA in HNSCC primary tumors identifies patients at high risk for recurrence. In these tumors, progression could rely on the Hippo-YAP pathway instead of the canonical Akt/mTOR pathway. This observation could have important implications in the therapeutic options for patients.

2018-04-02 | GSE95805 | GEO

Single-cell Sequencing Analysis Identifies Intratumoral Cell Population in Head and Neck Squamous Cell Carcinoma from 4NQO-induced Mice upon anti-CD276 Therapy

Project description:In this study, we aimed to identifies the landscape alterations of intratumoral cell population in HNSCC from 4NQO-induced mice upon anti-CD276 treatment by using single cell sequencing analysis.we characterized the alterations of intratumoral cell population by separating cancer cells and yielded 6 distinct cancer cell subpopulations defined by the transcriptional state of cells and known marker genes, including the sunpopulation with pEMT, stress, typical epithelial differentiation, high cell-cycling, metabolism and immune fetures. In response of CD276 treatment, the frequecey of cells with pEMT, cell cycling and immune features are dcreased as compared to the vehicle control mice.

2021-05-28 | GSE164817 | GEO

Phosphoproteomic analysis of breast epithelial cells with isogenic knockin of PIK3CA mutations

Project description:The PIK3CA gene is frequently mutated in human cancers. To study the signaling mechanisms responsible for cell growth and invasion phenotypes induced by mutant PIK3CA molecules, we carried out a SILAC-based quantitative phosphoproteomic analysis of MCF10A, a spontaneously immortalized normal mammary epithelial cell line, and two MCF10A knockin cell lines containing different activating mutations of the PIK3CA gene. MCF10A and PIK3CA mutation knock in cells were propagated in DMEM/F12 SILAC media deficient in both L-lysine and L-arginine and supplemented with light lysine (K) and arginine (R) for light, 2H4-K and 13C6-R for medium state and 13C615N2-K and 13C615N4-R for heavy state labeling. Cell lysates were prepared in urea lysis buffer containing 20 mM HEPES pH 8.0, 9 M urea, 1 mM sodium orthovanadate, 2.5 mM sodium pyrophosphate, 1 mM ß-glycerophosphate and 5mM sodium fluoride. The lysates were reduced, alkylated and digested by trypsin. Tryptic peptides were desalted by C18 reverse phase column and followed by strong cation exchange (SCX) fractionation. Fractionated peptides were subjected to TiO2-based phosphopeptide enrichment. LC-MS/MS analysis of enriched phosphopeptides was carried out using a reverse-phase liquid chromatography system interfaced with an LTQ-Orbitrap Velos mass spectrometer. Proteome Discoverer (v 1.3) suite was used for quantitation and database searches. The tandem mass spectrometry data were searched using Mascot (2.2.0) and SEQUEST search algorithms against a Human RefSeq database supplemented with frequently observed contaminants.

2015-07-28 | PXD000599 | Pride

Activating Mutations in PIK3CA result in Widespread Modulation of the Tyrosine Phosphoproteome

Project description:The human oncogene PIK3CA is frequently mutated in human cancers. The two hotspot mutations in PIK3CA, E545K and H1047R, have been shown to regulate widespread signaling events downstream of AKT. However, the impact of these activating mutations on the tyrosine phosphorylation signaling in the cell has not been studied. Here, we performed a global phosphotyrosine profiling using isogenic knockin cell lines containing these activating mutations. We identified 824 unique phosphopeptides from 308 proteins. We found a surprisingly widespread modulation of tyrosine phosphorylation levels of proteins in the knockin mutant cells, with many of the regulated proteins involved in important biological processes, including those in the cytoskeletal migration pathways and kinase regulated signaling. We observed a widespread modulation of the tyrosine kinome, with 24 of the tyrosine kinases showing either upregulation or downregulation in phosphorylation levels. Many of the regulated phosphosites that we identified were located in the kinase domain or the canonical activating sites, indicating that the kinases were active and hence their downstream signaling pathways. Our study thus shows that the activating mutations in PIK3CA result in widespread tyrosine signaling regulation, in addition to the serine/threonine signaling pathways activated by the canonical PI3K-AKT axis.

2018-10-24 | PXD001460 | Pride

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