Phosphotyrosine phosphatase R3 receptors: Origin, evolution and structural diversification

Chicote, Javier U.; DeSalle, Rob; Garcı́a-España, Antonio

doi:10.1371/journal.pone.0172887

Cited by 9 publications

(9 citation statements)

References 46 publications

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“…PTPRO belongs to the R3 subtype family of receptor-type protein tyrosine phosphatase, the expression of which has been found to be reduced in several types of cancer, such as LSCC, breast cancer, and hepatocellular carcinoma. [33][34][35][36][37] PTPRO functions as a tumor suppressor because it is often silenced by DNA hypermethylation. 34 Apart from this, PTPRO inhibits tumorigenesis probably by suppressing cell proliferation and facilitating apoptosis.…”

Section: Discussionmentioning

confidence: 99%

LncRNA HULC promotes lung squamous cell carcinoma by regulating PTPRO via NF‐κB

Xu¹,

Li²,

Wang

et al. 2019

J of Cellular Biochemistry

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Accumulating studies have implicated that long noncoding RNA (lncRNA) plays a vital role in lung cancer. However, little is known of the role of lncRNA highly upregulated in liver cancer (HULC) in the pathogenesis of lung squamous cell carcinoma (LSCC). In this study, we investigated the modifying effects and underlying mechanisms of lncRNA HULC in LSCC. Significantly decreased level of lncRNA HULC was observed in LSCC samples compared with adjacent tissues. Besides, the expression of lncRNA HULC was negatively associated with protein tyrosine phosphatase receptor type O (PTPRO) in LSCC. Moreover, lncRNA HULC could promote the proliferation of LSCC cells by downregulating the expression PTPRO dependent on the phosphorylation and activation of nuclear factor-κB (NF-κB). The present study firstly shows strong evidence supporting a critical role of lncRNA HULC in promoting LSCC by regulating PTPRO/NF-κB signaling pathway, which provides new promising biomarkers for LSCC. K E Y W O R D S long noncoding RNA, lung cancer, nuclear factor-κB, protein tyrosine phosphatase receptor type O

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Section: Discussionmentioning

confidence: 99%

LncRNA HULC promotes lung squamous cell carcinoma by regulating PTPRO via NF‐κB

Xu¹,

Li²,

Wang

et al. 2019

J of Cellular Biochemistry

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“…Protein tyrosine phosphorylation is a critical regulatory event that is involved in almost all aspects of cellular function, and its deregulation leads to health disorders, including cancer ( 4 , 5 ). Protein tyrosine phosphorylation is a reversible and dynamic process positively regulated by protein tyrosine kinases (PTKs) and negatively regulated by protein tyrosine phosphatases (PTPs) ( 5 , 6 ). The human genome encodes 107 PTPs that catalyze the removal of phosphate groups from tyrosine residues ( 4 , 5 ).…”

Section: Introductionmentioning

confidence: 99%

“…Protein tyrosine phosphorylation is a reversible and dynamic process positively regulated by protein tyrosine kinases (PTKs) and negatively regulated by protein tyrosine phosphatases (PTPs) ( 5 , 6 ). The human genome encodes 107 PTPs that catalyze the removal of phosphate groups from tyrosine residues ( 4 , 5 ). They directly rival the actions of PTKs.…”

Section: Introductionmentioning

confidence: 99%

PTPRO predicts patient prognosis and correlates with immune infiltrates in human clear cell renal cell carcinoma

Gan¹,

Zhang²

2020

Transl Cancer Res TCR

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Background: The tumor-suppressive role of protein tyrosine phosphatase receptor type O (PTPRO) has been described in a variety of human cancers; however, the clinical significance of PTPRO in human clear cell renal cell carcinoma (ccRCC) remains unclear.Methods: PTPRO expression in renal cell carcinoma (RCC) was analyzed via the Oncomine database, Gene Expression Omnibus (GEO) datasets, and The Cancer Genome Atlas (TCGA) datasets. The Kaplan-Meier curves and Cox proportional hazards model were used to evaluate the relationship of PTPRO with overall survival in ccRCC. Gene ontology (GO) analysis and gene set enrichment analysis (GSEA) were performed to explore the signaling pathways in which PTPRO may be involved. The correlation between PTPRO and immune infiltrates in ccRCC was investigated via Tumor Immune Estimation Resource (TIMER) database. The association between PTPRO mRNA expression and its methylation in RCC was analyzed using the Cancer Cell Line Encyclopedia (CCLE) dataset, GEO dataset, and cBioPortal database.The impact of PTPRO methylation on overall survival was estimated by the MethSurv database.Results: We showed that the expression of PTPRO was significantly lower in human RCC. Moreover, the lower expression of PTPRO was associated with worse overall survival in ccRCC, particularly in the advanced stage patients. Multivariate Cox regression analysis revealed the expression of PTPRO as an independent prognostic predictor for overall survival of ccRCC. Of note, PTPRO was found to be associated with the activation of immune signaling and immune cell infiltration. Furthermore, methylation of PTPRO was prevalently observed in ccRCC, and methylation of PTPRO predicted the poor outcome of ccRCC.Conclusions: Our findings suggested that PTPRO at both RNA and DNA methylation levels had the potential as a prognostic biomarker for predicting prognosis, and PTPRO expression was closely associated with immune infiltration in ccRCC patients.

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“…All sequences used in this study were checked for errors and curated manually. Data mining was performed as previously described by [50,51]. We searched the NCBI protein database with the BLASTP program using as a bait known human oncoproteins [52].…”

Section: Data Mining and Sequence Analysismentioning

confidence: 99%

Origin and evolution of RAS oncoprotein membrane targeting

Philips

Garcı́a-España²

2023

Preprint

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KRAS, HRAS and NRAS oncogenes belong to a family of 40 highly homologous genes, which in turn are a subset of a superfamily of >160 genes encoding small GTPases. RAS oncoproteins consist of a globular G-domain (aa1-166) and a 22-23aa unstructured hypervariable region (HVR) that mediates membrane targeting. The evolutionarily origins of the RAS isoforms, their HVRs and alternative splicing of the KRAS locus has not been explored. We found that KRAS is basal to the oncogene family and its duplication generated HRAS in the common ancestor of vertebrates. In a second round of duplication HRAS generated NRAS and KRAS generated an additional RAS gene we have designated KRASBL, absent in mammals and birds. KRAS4A arose through a duplication and insertion of the 4th exon of NRAS into the 3rd intron of KRAS. We found evolutionarily conservation of a short polybasic region (PBR1) in HRAS, NRAS and KRAS4A, a second polybasic region (PBR2) in KRAS4A, two neutralized basic residues (NB) and a serine in KRAS4B and KRASBL, and a modification of the CaaX motif in vertebrates with farnesyl rather than geranylgeranyl polyisoprene lipids, suggesting that a less hydrophobic membrane anchor is critical to RAS oncoprotein function. The persistence of four RAS isoforms through >400 MY of evolution argues strongly for differential function.

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Phosphotyrosine phosphatase R3 receptors: Origin, evolution and structural diversification

Cited by 9 publications

References 46 publications

LncRNA HULC promotes lung squamous cell carcinoma by regulating PTPRO via NF‐κB

LncRNA HULC promotes lung squamous cell carcinoma by regulating PTPRO via NF‐κB

PTPRO predicts patient prognosis and correlates with immune infiltrates in human clear cell renal cell carcinoma

Origin and evolution of RAS oncoprotein membrane targeting

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