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Identification of PTENα associated proteins under stress condictions in B16 cells by mass spectrometry

ABSTRACT: PTENα is the first isoform of tumor suppressor PTEN. To investigate the molecular mechanism by which PTENα modulates cell response to inflammation, we performed pull-down assays with FLAG-tagged proteins coupled with mass spectrometry under condition of H2O2 treatment in B16 cells.

ORGANISM(S): Mus Musculus

SUBMITTER: Yuxin Yin

PROVIDER: PXD040709 | iProX | Tue Jul 13 00:00:00 BST 2021

REPOSITORIES: iProX

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PTENα functions as an immune suppressor and promotes immune resistance in PTEN-mutant cancer.

Sun Yizhe Y Lu Dan D Yin Yue Y Song Jia J Liu Yang Y Hao Wenyan W Qi Fang F Zhang Guangze G Zhang Xin X Liu Liang L Lin Zhiqiang Z Liang Hui H Zhao Xuyang X Jin Yan Y Yin Yuxin Y

Nature communications 20210826 1

PTEN is frequently mutated in human cancers and PTEN mutants promote tumor progression and metastasis. PTEN mutations have been implicated in immune regulation, however, the underlying mechanism is largely unknown. Here, we report that PTENα, the isoform of PTEN, remains active in cancer bearing stop-gained PTEN mutations. Through counteraction of CD8<sup>+</sup> T cell-mediated cytotoxicity, PTENα leads to T cell dysfunction and accelerates immune-resistant cancer progression. Clinical analysis ...[more]

PMID: 34446716

Similar Datasets

Identification of PTENα associated proteins under stress condictions by mass spectrometry

Project description:PTENα is the first isoform of tumor suppressor PTEN. To investigate the molecular mechanism by which PTENα modulates cell response to inflammation, we performed pull-down assays with FLAG-tagged proteins coupled with mass spectrometry under condition of H2O2 treatment.

2020-10-03 | PXD021839 |

PTENa/b paradoxically promote carcinogenesis through WDR5-H3K4me3 axis

Project description:PTEN, a widely investigated tumor suppressor, has at least two longer translational variants, PTEN and . However, the regulation and precise roles of endogenous PTEN/ in tumorigenesis remain greatly unknown. Here we show that USP9X and FBXW11 selectively regulate the stability of PTEN/ but not PTEN proteins by deubiqitination and ubiquitination respectively. USP9X promotes and FBXW11 suppresses tumorigenesis mediated by PTEN/. In contrast to the current paradigm for PTEN as a tumor suppressor, PTEN/ promote tumorigenesis of cancer cells in a phosphatase-independent manner. Mechanistically, PTEN/ localized in the nucleus regulate expressions of tumor-promoting genes such as NOTCH3 in the similar way as the H3K4 presenter WDR5. Further, PTEN/ but not PTEN directly interact with WDR5 to promote trimethylation of H3K4 and maintain a tumor-promoting signature. Taken together, our results indicate that PTEN/ are a double-edged sword for carcinogenesis, suggesting that reinterpretation of the importance of PTEN gene in carcinogenesis is warranted.

2019-11-14 | PXD013196 | Pride

A Novel PI3K Regulator, ARID4B, Presents Synthetic Essentiality in PTEN-deficient Prostate Cancer [ChIP-seq]

Project description:Phosphatase and tensin homologue (PTEN) is the most frequently mutated tumor suppressor gene in human prostate cancer. Synthetic essentiality is defined as cancer that harbors a specific tumor suppressor deficiency is dependent on synthetic-essential genes for the malignant phenotypes. Recently, targeting such synthetic-essential genes has become an attractive treatment approach for cancers that acquire loss-of-function mutations in tumor suppressor genes. Here, we show that AT-rich interaction domain 4B (ARID4B) functions as a synthetic-essential gene in prostate tumorigenesis driven by PTEN deficiency. This functional interaction between ARID4B and PTEN is recapitulated in the mouse model carrying prostate-specific deletions of Pten and Arid4b in which ablation of ARID4B attenuated prostate cancer progression elicited by loss of PTEN. Although the tumor suppressor function of PTEN is most attributed to its lipid phosphatase activity that counters the PI3K action in cytoplasm, we identified the PTEN-ARID4B-PI3K axis in which nuclear PTEN inhibits expression of ARID4B, while ARID4B serves as a transcriptional activator of the PI3K subunits PIK3CA and PIK3R2 to trigger the PI3K/AKT pathway. Our study further demonstrated that the reciprocal binding of ARID4B and histone H1 to the PIK3CA and PIK3R2 promoters modulates chromatin condensation, indicating a mechanism by which ARID4B activates these promoters. Finally, a three-gene signature consisting of PTEN, ARID4B, and PI3K substantially improves the predictive power for tumor recurrence in human prostate cancer patients, underscoring the clinical significance of this newly identified PTEN-ARID4B-PI3K axis. These findings reveal a novel synthetic-essential relationship between ARID4B and PTEN, thus exposing a previously unidentified cancer-specific vulnerability, and supporting ARID4B as a potential therapeutic target for prostate cancer patients with PTEN mutations.

2019-08-23 | GSE116669 | GEO

A Novel PI3K Regulator, ARID4B, Presents Synthetic Essentiality in PTEN-deficient Prostate Cancer [RNA-seq]

2019-08-23 | GSE116668 | GEO

ChIP-seq of wild-type SOX18 and a dominant-negative variant (SOX18RaOp) in HeLa cells

Project description:We investigated differences in the chromatin-binding profile of SOX18 (mouse) and its dominant-negative isoform SOX18RaOp, and how SOX18RaOp alters the binding location of SOX18. HeLa cells were transfected to generate 3 different conditions: 1. myc-SOX18, 2. myc-SOX18RaOp and 3. myc-SOX18 with untagged-SOX18RaOp. Each condition was performed in duplicate (6 samples total). An anti-Myc antibody was used to perform the pull-down. Background (input) was assessed by pooling cells transfected with each condition and sequencing without immunoprecipitation.

2021-08-30 | E-MTAB-10609 | biostudies-arrayexpress

PTENε, a new isoform of PTEN, suppresses tumor metastasis through filopodia formation regulation.

Project description:PTEN is frequently mutated in a wide range of malignancies. Beyond suppressing tumorigenesis, PTEN is involved in multiple biological processes, and the complexity of PTEN function is partially attributed to PTEN family members including PTENα and PTENβ. Here, we report the identification of PTENε (also named as PTEN5), a novel N-terminal-extended PTEN isoform that suppresses tumor invasion and metastasis. We show that the translation of PTENε is initiated from the CUG816 codon within the 5’UTR region of PTEN mRNA. PTENε mainly localizes in the cell membrane, and physically associates with and dephosphorylates VASP and ACTR2, which govern filopodia formation and cell motility. We found that endogenous depletion of PTENε promotes filopodia formation and enhances the metastasis capacity of tumor cells. Overall, we identify a new isoform of PTEN with distinct localization and function compared to the known members of the PTEN family. These findings enrich the PTEN family constitution and advance our current understanding of the importance and diversity of PTEN functions.

2021-01-11 | PXD022245 | Pride

Next Generation Sequencing Facilitates Quantitative Analysis of RNAs bound by DDX5 and RORgt in cultured T helper 17 cell [RIP-seq]

Project description:Purpose: The goals of this study are to compare RNAs bound by DDX5 and RORgt in cultured T helper 17 cell in wildtype background. Methods: Th17 mRNA profiles of 48hrs in vitro cultured T helper 17 cells from wild-type mice were generated by deep sequencing, using Illumina HighSeq. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: BurrowsâWheeler Aligner (BWA) and TopHat followed by CuffDiff. qRTâPCR validation was performed using SYBR Green assays. Results: Among the 3444 RefSeq non-coding RNAs and 46449 NONCODE non-coding RNAs, 2533 were found to be expressed in Th17 cells (FPKM>1). 210 of them were enriched in DDX5 pull-down and 119 of them were enriched in RORgt pull-down. Conclusions: Our study suggest that a subset of 31 ncRNAs were co-enriched in DDX5 and RORgt pull-down. DDX5 or RORgt-associated-RNA profiles of 48hr in vitro cultured Th17 from wild type (WT) mice were generated by deep sequencing using Illumina HighSeq

2015-12-21 | E-GEOD-70109 | biostudies-arrayexpress

PTEN regulated PI3K-p110 and AKT isoform plasticity controls metastatic prostate cancer progression

Project description:PTEN loss, one of the most frequent mutations in prostate cancer (PC), is presumed to drive disease progression through AKT activation. However, two transgenic PC models with Akt activation plus Rb loss exhibited different metastatic development: Pten/RbPE:-/- mice produced systemic metastatic adenocarcinomas with high AKT2 activation, whereas RbPE:-/- mice deficient for the Src-scaffolding protein, Akap12, induced high-grade prostatic intraepithelial neoplasias and indolent lymph node dissemination, correlating with upregulated phosphotyrosyl PI3K-p85α. Using PC cells isogenic for PTEN, we show that PTEN-deficiency correlated with dependence on both p110β and AKT2 for in vitro and in vivo parameters of metastatic growth or motility, and with downregulation of SMAD4, a known PC metastasis suppressor. In contrast, PTEN expression, which dampened these oncogenic behaviors, correlated with greater dependence on p110α plus AKT1. Our data suggest that metastatic PC aggressiveness is controlled by specific PI3K/AKT isoform combinations influenced by divergent Src activation or PTEN-loss pathways.

2023-11-01 | GSE242387 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of RNAs bound by DDX5 and RORgt in cultured T helper 17 cell [RIP-seq]

Project description:Purpose: The goals of this study are to compare RNAs bound by DDX5 and RORgt in cultured T helper 17 cell in wildtype background. Methods: Th17 mRNA profiles of 48hrs in vitro cultured T helper 17 cells from wild-type mice were generated by deep sequencing, using Illumina HighSeq. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) and TopHat followed by CuffDiff. qRT–PCR validation was performed using SYBR Green assays. Results: Among the 3444 RefSeq non-coding RNAs and 46449 NONCODE non-coding RNAs, 2533 were found to be expressed in Th17 cells (FPKM>1). 210 of them were enriched in DDX5 pull-down and 119 of them were enriched in RORgt pull-down. Conclusions: Our study suggest that a subset of 31 ncRNAs were co-enriched in DDX5 and RORgt pull-down.

2015-12-21 | GSE70109 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of RNAs bound by DDX5 and RORgt in cultured T helper 17 cell [ChIRP-Seq]

Project description:Purpose: The goals of this study are to compare RNAs bound by DDX5 and RORgt in cultured T helper 17 cell in wildtype background. Methods: Th17 mRNA profiles of 48hrs in vitro cultured T helper 17 cells from wild-type mice were generated by deep sequencing, using Illumina HighSeq. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) and TopHat followed by CuffDiff. qRT–PCR validation was performed using SYBR Green assays. Results: Among the 3444 RefSeq non-coding RNAs and 46449 NONCODE non-coding RNAs, 2533 were found to be expressed in Th17 cells (FPKM>1). 210 of them were enriched in DDX5 pull-down and 119 of them were enriched in RORgt pull-down. Conclusions: Our study suggest that a subset of 31 ncRNAs were co-enriched in DDX5 and RORgt pull-down.

2015-12-21 | GSE73912 | GEO

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