scholarly journals Protein tyrosine phosphatase, receptor type B is a potential biomarker and facilitates cervical cancer metastasis via epithelial-mesenchymal transition

Bioengineered ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 5739-5748
Author(s):  
Zhuo-Ya Huang ◽  
Peng-Juan Liao ◽  
Ying-xia Liu ◽  
Ming Zhong ◽  
Ai-hua Sun ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Protein Tyrosine Phosphatase ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Tyrosine Phosphatase ◽  
Receptor Type ◽  
Type B ◽  
Mesenchymal Transition ◽  
Protein Tyrosine ◽  
Potential Biomarker

scholarly journals The protein tyrosine phosphatase Pez regulates TGFβ, epithelial–mesenchymal transition, and organ development

2007 ◽  
Vol 178 (7) ◽  
pp. 1223-1235 ◽  
Author(s):  
Leila Wyatt ◽  
Carol Wadham ◽  
Lesley A. Crocker ◽  
Michael Lardelli ◽  
Yeesim Khew-Goodall
Keyword(s):  
Protein Tyrosine Phosphatase ◽  
Crucial Role ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Mdck Cells ◽  
Tyrosine Phosphatase ◽  
Pharyngeal Arches ◽  
Mesenchymal Transition ◽  
Protein Tyrosine ◽  
And Function

Epithelial–mesenchymal transition (EMT), crucial during embryogenesis for new tissue and organ formation, is also considered to be a prerequisite to cancer metastasis. We report here that the protein tyrosine phosphatase Pez is expressed transiently in discrete locations in developing brain, heart, pharyngeal arches, and somites in zebrafish embryos. We also find that Pez knock-down results in defects in these organs, indicating a crucial role in organogenesis. Overexpression of Pez in epithelial MDCK cells causes EMT, with a drastic change in cell morphology and function that is accompanied by changes in gene expression typical of EMT. Transfection of Pez induced TGFβ signaling, critical in developmental EMT with a likely role also in oncogenic EMT. In zebrafish, TGFβ3 is co- expressed with Pez in a number of tissues and its expression was lost from these tissues when Pez expression was knocked down. Together, our data suggest Pez plays a crucial role in organogenesis by inducing TGFβ and EMT.

Effect of arsenic trioxide on epithelial-mesenchymal transition via induction of SH2?containing protein tyrosine phosphatase 1.

2017 ◽  
Vol 35 (4_suppl) ◽  
pp. 76-76
Author(s):  
Jong-Jae Park ◽  
Moon Kyung Joo ◽  
Hyo Soon Yoo ◽  
Beom Jae Lee ◽  
Taehyun Kim ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Protein Tyrosine Phosphatase ◽  
Epithelial Mesenchymal Transition ◽  
Tyrosine Phosphatase ◽  
Dependent Manner ◽  
Gastric Cancer Cells ◽  
Mesenchymal Transition ◽  
Protein Tyrosine ◽  
Dose Dependent

76 Background: Arsenic trioxide (ATO) is known to inhibit epithelial-mesenchymal transition (EMT) in hepatolocellular carcinoma and breast cancer cells, however, little has been reported in gastric cancer cells. In this study, we aimed to investigate the mechanism of ATO to inhibit signal transducer and activator of transcription 3 (STAT3) activity and EMT in gastric cancer cells. Methods: We performed wound closure assay and Matrigel invasion assay for functional studies of EMT, and western blot for measurement of protein markers using AGS gastric cancer cells. Results: Compared with control, 5 and 10 μM of ATO significantly inhibited cellular migration and inhibition in a dose-dependent manner. Furthermore, ATO significantly downregulated snail expression, a mesenchymal marker, and upregulated E-cadherin expression, an epithelial marker. We could observe that ATO induced SH2-containing protein tyrosine phosphatase 1 (SHP1), a non-receptor type protein tyrosine phosphatase, and subsequently downregulated phospho-STAT3 in a dose-dependent manner. To validate the molecular link between ATO and SHP1 to inhibit EMT in gastric cancer cell, we pre-treated 50 μM of pervanadate, a phosphatase inhibitor, before treatment of 10 μM ATO, and this significantly abolished anti-invasive effect by ATO in AGS cells. In xenograft tumor model, intraperitoneal injection of ATO significantly reduced the tumor volume and upregulated SHP-1 expression by immunohistochemistry stain compared with vehicle, which were reversed by ATO with pervanadate injection. Conclusions: Our findings suggest that ATO may show anti-EMT effects via induction of SHP1 and inhibition of STAT3 activity in gastric cancer cells.

Effect of PTPRB on metastasis of colorectal carcinoma and induction of epithelial-mesenchymal transition.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e15099-e15099
Author(s):  
Xingyue Weng ◽  
Shu Zheng
Keyword(s):  
Cell Lines ◽  
Protein Tyrosine Phosphatase ◽  
Epithelial Mesenchymal Transition ◽  
Tyrosine Phosphatase ◽  
Multiple Cancer ◽  
Vimentin Expression ◽  
Term Survival ◽  
Mesenchymal Transition ◽  
Protein Tyrosine ◽  
E Cadherin

e15099 Background: Colorectal cancer (CRC) is one of the most common and lethal cancers worldwide. Metastasis and recurrence are believed to be responsible for limiting long-term survival of patients with CRC. Protein tyrosine phosphatase, receptor type B ( PTPRB) belongs to the protein tyrosine phosphatase family. Multiple studies have previously demonstrated that dysregulation of PTPRB function and expression has been shown to correlate with carcinogenesis and tumor progression in multiple cancer types. Methods: In this study, we used CRC cell lines to explore the expression of PTPRB and to analyze the biological function of PTPRB protein. Surgical tumor specimens were collected for immunohistochemical staining to evaluate PTPRB expression.Real-time polymerase chain reaction (PCR) and western blot analysis were used to confirm genes and proteins of interest, respectively. Results: PTPRB is expressed at significantly higher levels in CRC tissues compared to adjacent non-tumor tissues and in CRC cell lines with high metastasis potential. PTPRB knockdown decreased the number of invasive CRC cells in a vitro wound healing model, and also reduced tumor metastasis in vivo. Conversely, PTPRB overexpression decreased E-cadherin expression and promoted vimentin expression, while PTPRB knockdown had the opposite effect. Hypoxic conditions induced EMT and promoted metastasis in CRC cells, but these effects were eliminated by PTPRB knockdown. EMT blockade via TWIST1 knockdown inhibited the migration and invasiveness of CRC cells, and even increased PTPRB expression could not reverse this effect. Conclusions: PTPRB is upregulated in CRC and overexpression of PTPRB promotes the metastasis of CRC. Moreover, our study revealed the effect of PTPRB on promoting EMT, as reflected in increased vimentin and decreased E-cadherin expression. PTPRB is a novel therapeutic target for the treatment of CRC.

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