Tumor microenvironment plays very important roles in the carcinogenesis. A variety of stromal cells in the microenvironment have been modified to support the unique needs of the malignant state. This study was to discover stromal differentially expressed proteins (DEPs) that were involved in colon carcinoma carcinogenesis. Laser capture microdissection (LCM) was captured and isolated the stromal cells from colon adenocarcinoma (CAC) and non-neoplastic colon mucosa (NNCM) tissues, respectively. Seventy DEPs were identified between the pooled LCM-enriched CAC and NNCM stroma samples by iTRAQ-based quantitative proteomics. Gene Ontology (GO) relationship analysis revealed that DEPs were hierarchically grouped into 10 clusters, and were involved in multiple biological functions that were altered during carcinogenesis, including extracellular matrix organization, cytoskeleton, transport, metabolism, inflammatory response, protein polymerization, and cell motility. Pathway network analysis revealed 6 networks and 56 network eligible proteins with Ingenuity pathway analysis. Four significant networks functioned in digestive system development and its function, inflammatory disease, and developmental disorder. Eight DEPs (DCN, FN1, PKM2, HSP90B1, S100A9, MYH9, TUBB, and YWHAZ) were validated by Western blotting, and four DEPs (DCN, FN1, PKM2, and HSP90B1) were validated by immunohistochemical analysis. It is the first report of stromal DEPs between CAC and NNCM tissues. It will be helpful to recognize the roles of stromas in the colon carcinoma microenvironment, and improve the understanding of carcinogenesis in colon carcinoma. The present data suggest that DCN, FN1, PKM2, HSP90B1, S100A9, MYH9, TUBB, and YWHAZ might be the potential targets for colon cancer prevention and therapy.

Investigation into the highly conserved 14‑3‑3ε protein has become increasingly important in cell biology due to its involvement in cell survival signaling, cell cycle control and apoptosis. The 14‑3‑3ε protein has been found to exert an impact on the development of various tumor types. However, the functional role and the possible mechanism of 14‑3‑3ε in gastric cancer remains to be elucidated. A previous study by our group indicated a negative correlation between 14‑3‑3ε expression levels and gastric cancer tissue differentiation and a positive correlation between 14‑3‑3ε expression levels and tumor infiltration, lymph node metastasis and tumor, nodes and metastasis staging. In the present study, 14‑3‑3ε suppression in the SGC7901 gastric cancer cell line was demonstrated to inhibit cell proliferation in vitro and tumor growth in vivo and the cell cycle‑associated proteins cyclin E and p27kip1 may have contributed to this antitumor effect. The present study showed for the first time that reducing the expression of 14‑3‑3ε may inhibit the proliferation and progression of gastric cancer and inhibition of this protein may provide a potential strategy for gastric cancer therapy in the future.