Expression Of SCF And C-kit In Pancreatic Cancer And The Relationship With Clinical Parameters

Background and Objective:Pancreatic cancer is a malignant tumor with high degree of malignancy.Due to the occultity,high degree of malignancy,rapid progress,and limited diagnosis and treatment of pancreatic cancer,the current survival rate of pancreatic cancer is still less than 10%.Early diagnosis of pancreatic cancer is difficult,and early infiltration and metastasis are prone to occur.Neural infiltration is an independent prognostic factor affecting patient survival.The c-kit protein molecule,also known as CD117,is a type III tyrosine kinase receptor that binds to stem cell factor(SCF).SCF plays an important role in hematopoiesis,spermatogenesis,and melanogenesis.Binding of SCF to c-kit results in homodimerization of the receptor and autophosphorylation at the tyrosine residue.Activation of c-kit leads to activation of multiple signaling cascades,including RAS/ERK,PI3-kinase,Src kinase and JAK/STAT pathways.Recently,SCF/c-kit has been found to be associated with breast cancer,testicular cancer,prostate cancer,gastric cancer,and lung cancer.Therefore,we hope to determine the relationship between SCF and c-kit in pancreatic cancer to determine its relationship with specific clinical conditions.Methods:From 2016 to 2018,patients who were hospitalized and operated at the Affiliated Tumor Hospital of Zhengzhou University had complete case data.The detailed information is as follows: 56 cases of pancreatic cancer,histological type are pancreatic ductal adenocarcinoma,The TNM staging is in accordance with the standards of the Union for International Cancer Control(UICC).None of the 56 patients with pancreatic cancer underwent radiotherapy,chemotherapy,or other treatment before surgery.In addition,in this experiment,20 specimens of normal pancreatic tissue were selected from the specimen bank.These specimens were taken from patients with common cholangiocarcinoma undergoing pancreaticoduodenectomy.These specimens were used as a control group in clinical tissue specimen experiments.Afterwards,we performed the following operations: 1.ELLISA method was used to detect the expression of SCF in serum of normal control group and pancreatic cancer patients.2.Immunohistochemistry was used to detect the expression of SCF,c-kit and nerve in normal pancreatic tissue and pancreatic cancer tissues.3.Total RNA extraction and cDNA synthesis in normal pancreatic tissue and pancreatic cancer tissues.4.The expression of SCF and c-kit mRNA in normal pancreatic tissue and pancreatic cancer tissues was detected by PCR.5.Western blot was used to detect the expression of SCF and c-kit proteins in normal pancreatic tissue and pancreatic cancer tissues.6.Finally,the data were statistically analyzed using SPSS21.0 statistical software.The statistical methods used for comparison between groups were ?2 test and Fisher exact probability method.Results:1.SCF was expressed in the serum of the normal control group and the pancreatic cancer experimental group,and there was no significant difference between the twogroup(P > 0.05).2.There was no significant difference in the expression level of serum SCF between patients with pancreatic cancer and different TNM staging,and whether it was accompanied by abdominal pain,jaundice and weight loss(P > 0.05).3.C-kit was expressed in different degrees in normal pancreatic tissue and pancreatic cancer tissues.The average expression rate of normal pancreatic tissue was only 28%;However,the average expression rate in pancreatic cancer tissues was as high as 70%,The expression of c-kit in pancreatic cancer tissues was significantly higher than that in normal pancreatic tissues(P<0.05).4.We used RT-PCR and Western Blot to detect the expression levels of SCF and c-kit mRNA and protein in normal pancreatic tissue and pancreatic cancer tissues,respectively.The results of RT-PCR showed that there was a small amount of SCF gene expression in normal pancreatic tissue and pancreatic cancer tissues,and the mRNA level was very low,but there was no statistically significant difference between the two groups(P > 0.05);while the c-kit gene was The expression of c-kit mRNA in pancreatic cancer tissues was significantly higher than that in normal pancreatic cancer tissues(P < 0.05).Western Blot results showed that SCF protein expression was weak in normal pancreatic tissue and pancreatic cancer tissues,and there was no significant difference between the two groups(P > 0.05);c-kit protein was in normal pancreatic tissue and pancreatic cancer.The expression of c-kit protein in pancreatic cancer tissues was significantly higher than that in normal pancreatic tissues(P < 0.05).5.We used the immunohistochemical method to detect the protein gene product PGP9.5.We observed the staining of nerve tissue in pancreatic cancer tissue.The number and area of nerves were significantly higher than those of normal pancreatic tissue.At the same time,we also found that arrangement of the nerve is disordered inthe pancreatic cancer tissue.6.There was no significant relationship between the expression of SCF in pancreatic cancer tissues and the clinical features of gender,age,tumor size,lymph node metastasis,histological grade,different TNM staging,and presence or absence of abdominal pain(P>0.05).The expression of c-kit in pancreatic cancer tissues was closely related to tumor size,lymph node metastasis,different TNM staging,and presence or absence of abdominal pain(P<0.05),but not related with gender,age,tumor location,and different histological types(P>0.05).7.In 56 patients with pancreatic cancer,the positive expression of c-kit protein was highly correlated with neuroinfiltration,and the difference was statistically significant(P<0.05).Conclusion:1.SCF is expressed in serum,but not in pancreatic cancer.c-kit is stable in pancreatic cancer.2.The expression of c-kit is closely related to the size of pancreatic cancer,lymph node metastasis,TNM stage and abdominal pain.The expression of c-kit in pancreatic cancer is correlated with the neurological infiltration of pancreatic cancer.