PTPRA facilitates cancer growth and migration via the TNF‑α‑mediated PTPRA‑NF‑κB pathway in MCF‑7 breast cancer cells
- Canfeng Lin
- Shubo Xin
- Xiaoguang Huang
- Feiran Zhang
Affiliations: Department of Oncology, Shantou Central Hospital, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515041, P.R. China, Department of Pharmacy, Shantou Central Hospital, Shantou, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515041, P.R. China, Department of General Surgery, The First Affiliated Hospital of Shantou University Medical College, Shantou, Guangdong 515041, P.R. China
- Published online on: August 20, 2020 https://doi.org/10.3892/ol.2020.11992
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Protein tyrosine phosphatase receptor type A (PTPRA), one of the classic protein tyrosine phosphatases, is crucial for modulating tumorigenesis and metastasis in breast cancer; however, its functional mechanism has not fully elucidated. The present study assessed PTPRA expression and estimated its clinical impact on survival using the Gene Expression Profiling Interactive Analysis database (GEPIA). Growth curves, colony formations and Transwell assays were utilized to examine cell proliferation and migration. Additionally, luciferase reporter assays were used to examine the potential tumor signaling pathways targeted by PTPRA in HEK293T cells. Furthermore, quantitative PCR (qPCR) was utilized to confirm the transcriptional regulation of PTPRA expression. Bioinformatic analyses of data from GEPIA identified PTPRA overexpression in patients with breast cancer. The growth curve, colony formation and transwell experiments demonstrated that PTPRA upregulation significantly promoted the cell proliferation and migration of MCF‑7 breast cancer cells. In contrast, PTPRA knockdown significantly attenuated cell proliferation and migration. Mechanistic experiments revealed that the transcriptional activity of NF‑κB was higher compared with other classic tumor pathways when they were activated by PTPRA in HEK293T cells. Furthermore, the transcriptional activity of NF‑κB was altered in a PTPRA‑dose‑dependent manner. Additionally, following exposure to TNF‑α, PTPRA‑deficient MCF‑7 cells exhibited lower NF‑κB transcriptional activity compared with normal control cells. The results of the present study demonstrate that PTPRA overexpression accelerates inflammatory tumor phenotypes in breast cancer and that the TNF‑α‑mediated PTPRA‑NF‑κB pathway may offer novel insight into early diagnosis and optimum treatment for breast cancer.