Over‐expression of S100A2 in pancreatic cancer correlates with progression and poor prognosis

Abstract

Controversy exists regarding the clinical significance of S100A2 in the progression of tumours. In pancreatic cancer, little is known about the role of S100A2. The aim of this study was to clarify the clinical significance of S100A2 expression in pancreatic carcinogenesis. We microdissected invasive ductal carcinoma (IDC) cells from 22 lesions, pancreatic intraepithelial neoplasia (PanIN) cells from five lesions, intraductal papillary mucinous neoplasm (IPMN) cells from 38 lesions, pancreatitis-affected epithelial (PAE) cells from 16 lesions, and normal ductal cells from 18 normal pancreatic tissues. S100A2 expression in 14 pancreatic cancer cell lines, microdissected cells and formalin-fixed paraffin-embedded (FFPE) samples was examined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Microdissection analyses revealed that IDC cells expressed higher levels of S100A2 than did IPMN, PAE or normal cells (all comparisons, p < 0.007). Cell lines from metastatic sites expressed higher levels of S100A2 than those from primary sites. PanIN cells expressed higher levels of S100A2 than normal cells (p = 0.018). IDC cells associated with poorly differentiated adenocarcinoma expressed higher levels of S100A2 than did IDC cells without poorly differentiated adenocarcinoma (p = 0.006). Analyses of FFPE samples revealed that levels of S100A2 were higher in samples from patients who survived < 1000 days after surgery than in those from patients who survived > 1000 days (p = 0.043). Immunohistochemical analysis was consistent with qRT-PCR. S100A2 may be a marker of tumour progression or prognosis in pancreatic carcinogenesis and pancreatic cancer.

S100A14: Novel Modulator of Terminal Differentiation in Esophageal Cancer

“…6). S100 proteins are therefore involved in the process of terminal differentiation of human epidermis and have been implicated in cancer as altered expression levels of several S100 proteins have been reported to correlate with tumor differentiation including ESCCs (7)(8)(9)(10)(11)(12)(13)(14). We have recently reported on the role of the S100 family member, S100A14, in driving esophageal carcinogenesis, showing that extracellular S100A14 affects esophageal cancer cell proliferation and apoptosis via interaction with RAGE, and intracellular S100A14 regulates cell invasion by MMP2 in a p53-dependent manner (15,16).…”

S100A6 binds to annexin 2 in pancreatic cancer cells and promotes pancreatic cancer cell motility

“…The majority of patients die within 1 year of diagnosis (Ghaneh et al, 2007). A number of proteins of the S100 family, including S100A2, S100A4, S100A6, S100A11 and S100P have been shown to be overexpressed in pancreatic cancer Shekouh et al, 2003;Vimalachandran et al, 2005;Ohuchida et al, 2006Ohuchida et al, , 2007a. In many cases, overexpression has been associated with enhanced invasion (Ohuchida et al, 2005;Suemizu et al, 2007;Whiteman et al, 2007) or poorer outcome (Vimalachandran et al, 2005;Oida et al, 2006;Ohuchida et al, 2007a).…”

S100A2 promoter-driven conditionally replicative adenovirus targets non-small-cell lung carcinoma

“…28 --31 Furthermore, overexpression of S100A2 was identified as a potential prognostic marker for poor disease-specific survival in patients with stage I NSCLC and pancreatic cancer. 9,11 Hypermethylation of the promoter region is a common mechanism of gene silencing. 32 --36 Site-specific DNA methylation of the S100A2 gene promoter in tumorigenic breast cancer cell lines has been shown to correlate with S100A2 repression during breast cancer progression.…”