title: The clinicopathological significance of REIC expression in colorectal carcinomas.
abstract: REIC is down-regulated in immortalized cell lines compared with the parental normal counterparts, and could inhibit colony formation, tumor growth and induce apoptosis. Here, its expression was examined by immunohistochemistry on tissue microarray containing colorectal non-neoplastic mucosa (NNM), adenoma and adenocarcinoma. Colorectal carcinoma tissue and cell lines were studied for REIC expression or its secretory level by Western blot, RT-PCR or enzyme-linked immunosorbent assay (ELISA). The results demonstrated that REIC was differentially expressed in Colo201, Colo205, DLD-1, HCT-15, HCT-116, HT-29, KM-12, SW480, SW620, and WiDr with its secretion concentration less than 300 pg/mL. Carcinomas showed statistically lower REIC expression than matched NNM with no difference for protein content. Immunohistochemically, REIC expression was significantly decreased from NNM, adenoma to adenocarcinoma (p<0.05). REIC expression was negatively correlated with depth of invasion, TNM staging, dedifferentiation, Capase-3 and nuclear inhibitor of growth 5 (ING5) expression (p<0.05), while not with age, sex, tumor size, lymphatic or venous invasion, or lymph node metastasis (p>0.05). Kaplan-Meier analysis indicated that REIC expression was not associated with the prognosis of colorectal carcinomas (p>0.05). Cox's analysis demonstrated that lymphatic and venous invasion, lymph node metastasis, and UICC staging were independent prognostic factors for carcinoma (p<0.05). Our study indicated that down-regulated REIC expression might play an important role in colorectal adenoma-adenocarcinoma sequence and subsequent progression. Aberrant REIC expression might be employed as a good marker of pathogenesis and development of colorectal carcinomas.
authors.affiliation: Department of Biochemistry and Molecular Biology, College of Basic Medicine, China Medical University, Shenyang, China.
authors.forename: W
authors.initials: W
authors.lastname: Wang
authors.forename: W
authors.initials: W
authors.lastname: Zhu
authors.forename: X-Y
authors.initials: XY
authors.lastname: Xu
authors.forename: X-C
authors.initials: XC
authors.lastname: Nie
authors.forename: X
authors.initials: X
authors.lastname: Yang
authors.forename: Y-N
authors.initials: YN
authors.lastname: Xing
authors.forename: M
authors.initials: M
authors.lastname: Yu
authors.forename: Y-P
authors.initials: YP
authors.lastname: Liu
authors.forename: Y
authors.initials: Y
authors.lastname: Takano
authors.forename: H-C
authors.initials: HC
authors.lastname: Zheng
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D000230:Adenocarcinoma / Q000235:genetics / Q000378:metabolism* / Q000401:mortality / Q000473:pathology; D000236:Adenoma / Q000235:genetics / Q000378:metabolism* / Q000401:mortality / Q000473:pathology; D014408:Biomarkers, Tumor / Q000235:genetics / Q000378:metabolism*; D015153:Blotting, Western; D018925:Chemokines; D015179:Colorectal Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000401:mortality / Q000473:pathology; D015536:Down-Regulation; D004797:Enzyme-Linked Immunosorbent Assay; D015972:Gene Expression Regulation, Neoplastic; D045325:HCT116 Cells; D019073:HT29 Cells; D006801:Humans; D007150:Immunohistochemistry; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism*; D053208:Kaplan-Meier Estimate; D015999:Multivariate Analysis; D009367:Neoplasm Staging; D011379:Prognosis; D016016:Proportional Hazards Models; D060888:Real-Time Polymerase Chain Reaction; D018570:Risk Assessment; D012307:Risk Factors; D046888:Tissue Array Analysis
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D014408:Biomarkers, Tumor; D018925:Chemokines; C498624:DKK3 protein, human; D036341:Intercellular Signaling Peptides and Proteins