PRSS3 is a prognostic marker in invasive ductal carcinoma of the breast

Abstract

ObjectiveSerine protease 3 (PRSS3) is an isoform of trypsinogen, and plays an important role in the development of many malignancies. The objective of this study was to determine PRSS3 mRNA and protein expression levels in invasive ductal carcinoma of the breast and normal surrounding tissue samples.ResultsBoth PRSS3 mRNA and protein levels were significantly higher in invasive ductal carcinoma of the breast tissues than in normal or benign tissues (all P < 0.05). High PRSS3 protein levels were associated with patients’ age, histological grade, Her-2 expression level, ki-67 expression, and the 5.0-year survival rate. These high protein levels are independent prognostic markers in invasive ductal carcinoma of the breast.Materials and MethodsWe used real-time quantitative polymerase chain reactions (N = 40) and tissue microarray immunohistochemistry analysis (N = 286) to determine PRSS3 mRNA and protein expression, respectively. PRSS3 protein levels in invasive ductal carcinoma of the breast tissues were correlated with the clinical characteristics of patients with invasive ductal carcinoma of the breast and their 5.0-year survival rate.ConclusionsPRSS3 acts as an oncogene in invasive ductal carcinoma of the breast development and progression. This finding implies that detection of PRSS3 expression can be a useful prognosis marker and the targeting of PRSS3 can potentially represent a new strategy for invasive ductal carcinoma of the breast treatment.

High‐level expression of PRSS3 correlates with metastasis and poor prognosis in patients with gastric cancer

“…However, in bladder, lung, and esophageal cancers, tumor occurrence and development are promoted by downregulation or silencing of PRSS3 expression . Furthermore, PRSS3 expression level is an independent predictor of prognosis in some tumors . To clarify the expression levels of PRSS3 in GC tissues, we assessed its expression in a tissue microarray constructed from matched samples of 175 patients with GC after radical resection (D2).…”

“…17,18,24 Furthermore, PRSS3 expression level is an independent predictor of prognosis in some tumors. [13][14][15][16] To clarify the expression levels of PRSS3 in GC tissues, we assessed its expression in a tissue microarray constructed from matched samples of 175 patients with GC after radical resection (D2). The results suggest that the expression of PRSS3 is higher in tumors than in normal adjacent tissues (P < 0.05), correlating with clinicopathological features of some cancer metastases.…”

“…PRSS3 is also widely expressed in many normal tissues, including the brain, lung, liver, and pancreas, suggesting a diversity of physiological functions aside from digestive activity; therefore, the function of PRSS3 in tumorigenesis may differ in various tumor types. High PRSS3 expression levels are found in cancers of the breast, ovarian epithelium, pancreas, and prostate . In lung and esophageal cancer, however, PRSS3 expression triggers downregulation of promoter hypermethylation, indicating suppressor gene activity .…”

“…High PRSS3 expression levels are found in cancers of the breast, ovarian epithelium, pancreas, and prostate. [13][14][15][16] In lung and esophageal cancer, however, PRSS3 expression triggers downregulation of promoter hypermethylation, indicating suppressor gene activity. 17,18 Nonetheless, the relation between PRSS3 expression and GC genesis and development remains unclear.…”

Circular RNA ADAM9 facilitates the malignant behaviours of pancreatic cancer by sponging miR-217 and upregulating PRSS3 expression

“…For example, PRSS3 was identified to be downregulated in non-small cell lung cancer and hepatocellular carcinoma [6,7]. On the contrary, high PRSS3 was found in epithelial ovarian cancer and breast cancer [8,9], implying that PRSS3 functions in a cell-or disease-context-dependent manner. Likewise, we previously observed that PRSS3 was remarkably increased in PC and promoted PC growth and metastasis by activating ERK/VEGF pathway [10].…”