AI Article Synopsis
- Elevated S100P expression is linked to colorectal cancer (CRC) metastasis and poor prognosis, being a more effective predictor than traditional markers like CEA and CA19-9.
- High S100P levels were shown to enhance the invasiveness and ability of CRC cells to metastasize, supported by experiments involving stable S100P knockdown and xenograft growth in mice.
- The process by which S100P promotes cancer progression involves activating the RAGE/ERK signaling pathway and inducing epithelial-mesenchymal transition (EMT), with RAGE being essential for this effect in colon cancer.
Article Abstract
Elevated expression of S100P has been detected in several tumor types. To analyze the potential use of S100P for the prediction of colorectal cancer (CRC) metastasis and prognosis, S100P expression was detected in 125 patients with colon adenocarcinoma by immunohistochemistry, followed by correlation and survival analysis. High S100P expression was correlated with metastasis, as demonstrated by clinically relevant data, and predicted poor survival more effectively than preoperative serum carcinoembryonic antigen (CEA) and carbohydrate antigen 19-9 (CA19-9) levels in colon adenocarcinoma. Stable S100P knockdown CRC cell lines were established to elucidate the relationship between S100P expression and tumor progression in vitro and in vivo. S100P knockdown resulted in reductions in the invasiveness and metastasis of CRC cells. Xenograft growth in nude mice also demonstrated that down-regulated S100P dramatically inhibited peritoneal metastasis of CRC cells. S100P promoted the invasion and metastasis of CRC by activating RAGE/ERK signaling and promoting the epithelial-mesenchymal transition (EMT). RAGE was found to be crucial for S100P-mediated EMT in colon cancer. Knockdown of RAGE in S100P-overexpressing colon cancer cells dramatically suppressed EMT process. Our results indicate that overexpression of S100P is related with an invasive and metastatic phenotype of CRC which is EMT-involved and RAGE dependent.
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| http://dx.doi.org/10.1016/j.cancergen.2016.02.002 | DOI Listing |
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