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

Bioengineered

Ai-hua Sun¹  Xiu-Ping Wang²  Xiao-cong Jiang²  Ying-xia Liu³  Ming Zhong³  Peng-Juan Liao⁴  Zhuo-Ya Huang⁴  Min Zhang⁵ 

[1] Department of Oncology, The Huizhou Municipal Central Hospital, Huizhou, Guangdong, Chin;Department of Oncology, The Huizhou Municipal Central Hospital, Huizhou, Guangdong, Chin;Department of Radiotherapy, The Huizhou Municipal Central Hospital, Huizhou, Guangdong, Chin;Department of Pathology, The First Hospital of Huizhou, Huizhou, Guangdong, Chin;Department of Pathology, The Huizhou Municipal Central Hospital, Huizhou, Guangdong, Chin;Department of Radiotherapy, The Huizhou Municipal Central Hospital, Huizhou, Guangdong, Chin;Department of Outpatient, The Huizhou Municipal Central Hospital, Huizhou, Guangdong, Chin;

关键词: PTPRB;    TCGA database;    cervical cancer;    biomarker;    metastasis;   

DOI  :  10.1080/21655979.2021.1968250

来源: Taylor & Francis

【 摘 要 】

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 tumor-suppressive 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 PTPRB-knockdown 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.

【 授权许可】

CC BY