Abstract
The role of PTPRT in breast cancer was not comprehensively explored and well analyzed. Our study comprehensively searched available databases to analyze the clinical role of PTPRT in breast cancer. We found PTPRT was an antioncogene and could be used to distinguish different stages, age groups, molecular types, and grades for breast cancer. PTPRT might be primary resistance biomarkers for taxane, anthracycline, and ixabepilone but not be acquired resistance biomarkers. Higher PTPRT expression levels were associated with longer overall survival and recurrence-free survival. PTPRT was negatively associated with Ki67 and CDK4/6 but positively associated with BCL-2. PTPRT might be associated with cell cycle and microtubule, and tumor infiltration in B cell and macrophage cell. PTPRT could predict chemotherapy effectiveness and prognosis for breast cancer patients. PTPRT might inhibit tumor growth via disrupting the microtubule dynamics and cell cycle in breast cancer.
Highlights
PTPRT belongs to the type IIB RPTP subfamily, which consisted of an extracellular domain, a transmembrane domain, a juxtamembrane region, and two phosphatase domains (D1 and D2) [1]
PTPRT plays in suppressing tumor growth and cell adhesion in various cancers, including colorectal cancer [2], hepatocellular carcinoma [3], prostate cancer [4], lung squamous cell carcinoma [5], esophageal squamous cell carcinoma [6], and glioma [7]
Zhang et al showed deletion of the fibronectin type III repeats (FNIII) of PTPRT result in defective cellcell aggregation, which suggest the inactivation of PTPRT might lead to cancer progression by disrupting cell-cell adhesion [9]
Summary
PTPRT belongs to the type IIB RPTP subfamily, which consisted of an extracellular domain (a meprin/A5/PTP μ domain, an Ig domain, and four fibronectin type III repeats), a transmembrane domain, a juxtamembrane region, and two phosphatase domains (D1 and D2) [1]. Five missense mutations in the most commonly altered PTPRT were found to reduce phosphatase activity, and expression of wild-type but not a mutant PTPRT in human cancer cells inhibited cell growth [8]. Zhang et al showed deletion of the fibronectin type III repeats (FNIII) of PTPRT result in defective cellcell aggregation, which suggest the inactivation of PTPRT might lead to cancer progression by disrupting cell-cell adhesion [9]. Zhang et al identified signal transducer and activator of transcription 3 (STAT3) as a substrate of PTPRT. They showed PTPRT dephosphorylated STAT3 at a tyrosine at amino acid Y705 and overexpression of normal PTPRT in colorectal cancer cells reduced the expression of STAT3 target genes [10]. In order to analyze the clinical role of PTPRT in breast cancer, we comprehensively searched available databases to summarize the treatment predictive and prognostic values of PTPRT
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