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

Abstract

Cervical cancer (CC) is one of the most common malignant tumors. This study analyzed the impact of protein tyrosine phosphatase, receptor type B (PTPRB) on malignant behavior of CC and explored its possible molecular mechanism. RT-PCR, western blot and Immunohistochemistry were applied to examine the expression of PTPRB in CC specimens and cells. Aberrant PTPRB expression in CC and survival outcomes were constructed using The Cancer Genome Atlas (TCGA) database and tissue microarray cervical squamous cell carcinoma cohort. Cultured human CC cells were assayed for viability, apoptosis, migration, and invasion in vitro and in vivo. Kyoto Encyclopedia of Genes and Genomes (KEGG) assays and gene set enrichment analysis (GSEA) assays were used to delve into PTPRB-related pathways using TCGA datasets. The levels of proteins associated with the epithelial-mesenchymal transition (EMT) pathway and modulated by PTPRB were examined through Western blot. We found that the levels of PTPRB in CC tissues and cells were distinctly up-regulated. PTPRB was also an unfavorable prognostic factor for CC patients. Functionally, PTPRB knockdown exhibits tumorsuppressive function via reducing cell proliferation and metastasis and inducing cell apoptosis. KEGG assays and GSEA assays suggested PTPRB overexpression was associated with several tumor-related pathways. The results of Western blot assays suggested that N-cadherin was decreased in the PTPRBknockdown CC cells, while E-cadherin was increased. Overall, PTPRB is highly expressed in CC and can effectively enhance the proliferation, metastasis and EMT process of tumor cells. PTPRB is expected to be a therapeutic target for CC.

Analysis of the Mutational Landscape of Osteosarcomas Identifies Genes Related to Metastasis and Prognosis and Disrupted Biological Pathways of Immune Response and Bone Development

“…Increased expression of PTPRQ was observed in metastatic tumors from mice [ 39 ]. Consistently, mutations resulting in the upregulation of other protein tyrosine phosphatase receptors have been implicated as a metastatic driver event in colorectal cancer [ 40 ] and cervical cancer [ 41 , 42 ]. Enhanced PTPRQ expression is described in the Human Protein Atlas (HPA) database ( , accessed on 11 May 2023) for several cancer groups, also including OS-derived cell lines.…”

Hsa_circ_0129047 sponges miR-665 to attenuate lung adenocarcinoma progression by upregulating protein tyrosine phosphatase receptor type B

“…PTPRB plays different roles in various cancers. PTPRB overexpression enhances the oncogenic phenotypes of cervical cancer in vitro [ 25 ], whereas it is poorly expressed in hepatocellular carcinoma and could weaken oncogenic Hippo signaling, mitigating tumor growth [ 26 ]. In addition, PTPRB was found to be a carcinogenic factor in NSCLC [ 20 ].…”

New molecular targets in canine hemangiosarcoma—Comparative review and future of the precision medicine

“…146 Several microRNA may act as PTPRB negative regulators, and their aberrant expression contributes to hepatocellular carcinoma, non-small cell lung cancer, and OSA development and progression, including metastases formation. [147][148][149] PTPRB is also thought to accelerate proliferation, metastases and epithelial-mesenchymal transition in cervical cancer 150 and its mutations were found in acinic cell carcinoma of the breast and lymphoma. 151,152 Due to those observations, PTPRB is expected to be a therapeutic target in some malignant tumours and may even mediate the therapeutic effects of radiotherapy in human thyroid carcinoma.…”