Expression And Clinical Significance Of ERp29 And E-cadherin In Colorectal Cancer

Background Colorectal cancer is one of the most common gastrointestinal cancer in China.The incidence of colorectal cancer is increasing annually,and the health burden can not be ignored.Colorectal tumorigenesis might result from multiple factors and genes.In spite of the understanding of colorectal cancer has been further developed through decades of extensive clinical and basic research.However,the potential mechanisms remain undefined,and further exploration is needed.Endoplasmic reticulum protein 29 is strongly associated with endoplasmic reticulum stress.Increassed proliferative,invasive and metastatic abilities induced by the deletion or mutation of endoplasmic reticulum protein 29 can promote tumor progression.Epithelial mesenchymal transition is important in the process of tumor cell invasion and metastasis.Downregulation of E-cadherin expression in protein levels is the most important molecular event in epithelial mesenchymal transition.Effects of endoplasmic reticulum protein 29 on colorectal tumoigensis remain unknown to date.Relationship between endoplasmic reticulum protein 29 and E-cadherin and the protein function in colorectal cancer need to be further explored.Objective To investigate the expression and function of endoplasmic reticulum protein 29 and E-cadherin in colorectal tumorigensis.To detect potential targets for further research by evaluating the relationship between endoplasmic reticulum protein 29 and E-cadherin preliminarily.Methods Colorectal cancer patients who recerved surgical treatment in our hospital during the past 2 years were collected.Data as to gender,age,tumor size,tumor differentiation,T staging,lymph nodes metastasis and TNM staging were also collected.Paraffin-embedded sections from 62 cases of colorectal cancer tissues were obtained and used for immunohistochemical staining of endoplasmic reticulum protein 29 and E-cadherin,respectively.The expression of endoplasmic reticulum protein 29 and E-cadherin in tumor tissues and adjacent tissues were compared.The clinical and pathological data of various levels of endoplasmic reticulum protein 29 and E-cadherin in patients with colorectal cancer were analyzed to to determine if there was a significant difference.And the correlationship between the expression of endoplasmic reticulum protein 29 and E-cadherin was investigated.Results 62 cases of colorectal cancer were collected,32 cases(51.61%)were male,average age was 64.44±11.99 years,30 cases were female(48.39%),average age was 59.70±11.11 years.The staining score of endoplasmic reticulum protein 29 was 0.93±1.01 in tumor tissues,and it was 4.03±2.04 in adjacent tissues,P < 0.05.The staining score of E-cadherin was 1.00±1.08 in tumor tissues,and it was 3.35±2.21 in adjacent tissues,P < 0.05.In all 62 cases of colorectal cancer,24 caces(38.70%)were positive expression of endoplasmic reticulum protein 29 and 38 caces(61.30%)were negative.There was a significant difference in TNM classification and lymph nodes metastasis between endoplasmic reticulum protein 29 positive group and negative group.In all 62 cases of colorectal cancer,15 caces(24.19%)were positive expression of E-cadherin and 47 caces(75.81%)were negative.There was a significant difference in tumor differentiation,TNM classification and lymph nodes metastasis between E-cadherin positive group and negative group.The kappa coefficient was 0.67 and R2 was 0.65 by analyzing the correlationship between the immunohistochemical staining scores of endoplasmic reticulum protein 29 and E-cadherin.Conclusion Colorectal cancer tissues show significantly lower expression levels of endoplasmic reticulum protein 29 and E-cadherin than adjacent tissues.The lower expression levels of endoplasmic reticulum protein 29 and E-cadherin,the lymph nodes metastasis are more common,and the tumor TNM classification may be wores.The invasive and metastatic propensity in colorectal cancer with low expression levels of endoplasmic reticulum protein 29 is more likely to be resulted from epithelial-mesenchymal transition associated with E-cadherin.