We are analyzing https://link.springer.com/article/10.1186/s12943-018-0803-3.

Title:
PTEN/PTENP1: ‘Regulating the regulator of RTK-dependent PI3K/Akt signalling’, new targets for cancer therapy | Molecular Cancer
Description:
Regulation of the PI-3 kinase (PI3K)/Akt signalling pathway is essential for maintaining the integrity of fundamental cellular processes, cell growth, survival, death and metabolism, and dysregulation of this pathway is implicated in the development and progression of cancers. Receptor tyrosine kinases (RTKs) are major upstream regulators of PI3K/Akt signalling. The phosphatase and tensin homologue (PTEN), a well characterised tumour suppressor, is a prime antagonist of PI3K and therefore a negative regulator of this pathway. Loss or inactivation of PTEN, which occurs in many tumour types, leads to overactivation of RTK/PI3K/Akt signalling driving tumourigenesis. Cellular PTEN levels are tightly regulated by a number of transcriptional, post-transcriptional and post-translational regulatory mechanisms. Of particular interest, transcription of the PTEN pseudogene, PTENP1, produces sense and antisense transcripts that exhibit post-transcriptional and transcriptional modulation of PTEN expression respectively. These additional levels of regulatory complexity governing PTEN expression add to the overall intricacies of the regulation of RTK/PI-3 K/Akt signalling. This review will discuss the regulation of oncogenic PI3K signalling by PTEN (the regulator) with a focus on the modulatory effects of the sense and antisense transcripts of PTENP1 on PTEN expression, and will further explore the potential for new therapeutic opportunities in cancer treatment.
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Keywords {🔍}

pten, pubmed, article, google, scholar, cas, cancer, cell, central, ptenp, regulation, protein, pseudogenes, pseudogene, gene, mutations, signalling, activity, growth, phosphatase, suppressor, pik, expression, kinase, pathway, receptor, function, wang, tumour, factor, domain, binding, nuclear, tumor, cellular, cancers, biol, pikakt, mechanisms, transcript, disease, major, regulatory, insulin, human, functional, mirnas, nat, zhang, antisense,

Topics {✒️}

cardiac ischemia/reperfusion injury rtk-dependent pi3k/akt signalling rkt-dependent pi3k/akt pathway rtk/pi3k/akt pathway continues rtk/pi3k/akt signalling pathway rtk-dependent pi3k/akt pathway proto-oncogenic pten-targeting intron pkb/akt-dependent cell survival article download pdf clear-cell renal carcinoma g-protein-coupled receptors pi3k-dependent akt signalling tumor-suppressive metabolic state clear-cell renal carcinomas pi3k/akt signalling pathway hmg-coa-reductase pseudogene ras-related nuclear protein pi3k/akt/mtor axis catalytically active open-conformation full size image pi3k/akt/mtor pathway drives pi3k/akt hyperactivation pi3k isoform-selective inhibitors pi3k-akt-mtor signaling small ubiquitin-related modifiers aggressive androgen-independent phenotypes short n-terminal sequence short n-terminal tail 3-phosphoinositide-dependent protein kinase n-terminal phosphatase domain pten-null xenograft tumors rtk/pi3k/akt regulation pi3k isoform-specific inhibitors universal ca2+−binding domain pi3k/akt/pten pathway generating pten-transgenic mice rtk//pi3k/akt activation post-translational regulatory mechanisms recruiting chromatin-repressor proteins post-translational regulatory mechanism pi3k/akt signalling pi3k/akt signalling [103] growth factor signaling /akt signalling pathway pseudogene-mediated posttranscriptional silencing pten/ptenp1 regulatory cycle overexpressing pten-specific mirnas small-cell lung cancer pi3k signalling pathway rtk signalling networks

Questions {❓}

A ceRNA hypothesis: the Rosetta stone of a hidden RNA language?
PTEN germline mutations in patients initially tested for other hereditary cancer syndromes: would use of risk assessment tools reduce genetic testing?
Phosphatase and tensin homolog (PTEN) pseudogene expression in endometrial cancer: a conserved regulatory mechanism important in tumorigenesis?
Pseudogenes: Pseudo or Real Functional Elements?
Pseudogenes: pseudo-functional or key regulators in health and disease?

Schema {🗺️}

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         description:Regulation of the PI-3 kinase (PI3K)/Akt signalling pathway is essential for maintaining the integrity of fundamental cellular processes, cell growth, survival, death and metabolism, and dysregulation of this pathway is implicated in the development and progression of cancers. Receptor tyrosine kinases (RTKs) are major upstream regulators of PI3K/Akt signalling. The phosphatase and tensin homologue (PTEN), a well characterised tumour suppressor, is a prime antagonist of PI3K and therefore a negative regulator of this pathway. Loss or inactivation of PTEN, which occurs in many tumour types, leads to overactivation of RTK/PI3K/Akt signalling driving tumourigenesis. Cellular PTEN levels are tightly regulated by a number of transcriptional, post-transcriptional and post-translational regulatory mechanisms. Of particular interest, transcription of the PTEN pseudogene, PTENP1, produces sense and antisense transcripts that exhibit post-transcriptional and transcriptional modulation of PTEN expression respectively. These additional levels of regulatory complexity governing PTEN expression add to the overall intricacies of the regulation of RTK/PI-3 K/Akt signalling. This review will discuss the regulation of oncogenic PI3K signalling by PTEN (the regulator) with a focus on the modulatory effects of the sense and antisense transcripts of PTENP1 on PTEN expression, and will further explore the potential for new therapeutic opportunities in cancer treatment.
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      headline:PTEN/PTENP1: ‘Regulating the regulator of RTK-dependent PI3K/Akt signalling’, new targets for cancer therapy
      description:Regulation of the PI-3 kinase (PI3K)/Akt signalling pathway is essential for maintaining the integrity of fundamental cellular processes, cell growth, survival, death and metabolism, and dysregulation of this pathway is implicated in the development and progression of cancers. Receptor tyrosine kinases (RTKs) are major upstream regulators of PI3K/Akt signalling. The phosphatase and tensin homologue (PTEN), a well characterised tumour suppressor, is a prime antagonist of PI3K and therefore a negative regulator of this pathway. Loss or inactivation of PTEN, which occurs in many tumour types, leads to overactivation of RTK/PI3K/Akt signalling driving tumourigenesis. Cellular PTEN levels are tightly regulated by a number of transcriptional, post-transcriptional and post-translational regulatory mechanisms. Of particular interest, transcription of the PTEN pseudogene, PTENP1, produces sense and antisense transcripts that exhibit post-transcriptional and transcriptional modulation of PTEN expression respectively. These additional levels of regulatory complexity governing PTEN expression add to the overall intricacies of the regulation of RTK/PI-3 K/Akt signalling. This review will discuss the regulation of oncogenic PI3K signalling by PTEN (the regulator) with a focus on the modulatory effects of the sense and antisense transcripts of PTENP1 on PTEN expression, and will further explore the potential for new therapeutic opportunities in cancer treatment.
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         Phosphatase and tensin homologue (PTEN)
         PTENP1
         Pseudogene
         Tyrosine kinase
         PI-3 kinase (PI3K)
         Cancer
         microRNA (miRNA)
         Cancer Research
         Oncology
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