Study Of The Relationship Between PTEN And C-myc Protein In Gastric Carcinoma

Objective: The occurrence and development of tumor is the result which themulti-stages,the multi-steps,the multi-genes affects mutually. The oncogeneactivation and anti-oncogene deactivation is the development foundation of each kindof tumor and plays the vital role in the developing process of the tumor ,affects thebiological behavior and decides the turnover and the prognosis of tumor . OncogeneC-myc expression product belongs to the serine/threonine phosphorylationprotein.The C-myc protein overexpression,which can cause the cell to be separatedfrom the normal fission track , speed up the multiplication,and induce the restingperiodcell to enter the cell division cycle, promote cell proliferation ,causes theoccurrence of tumor eventually. PTEN is thefirst discovered anti-oncogene which hasthe double specificity phosphatease activity until now.Through displays its proteintyrosine phosphataseand the lipin phosphatase activeness function, PTEN takes offtheessential activating enzymephosphate acid radical of the signal transductionpathway in the cell which many kinds of the lump growth factor leads,depresses itsphosphorylation level,blocks the signal conduction circuit, reduces its downstreamtarget gene expression product production , thus suppresses the cell growth ,transformation,adherency and migration,promotes the cell apoptosis. PTEN has thenegative regulative function of growth,invasion and the transfusion of tumorcell.About the respectively role which plays in the gastric cancer, the domesticandforeign scholars have done more thorough research.The research indicated that,theC-myc gene has close correlation with the gastric cancer occurrence and turnover,andplays the vital role in the regulation of tumor cell differentiation and tumor prognosisappraised, may take the independent prognosis target.PTEN is playing the vital role inthe gastric cancer cell differentiation and evolution process, may be a objective targetof the reflection of the gastric cancer biological behavior and the prognosis. Theoverseas research has demonstrated anti-oncogene PTEN overexpression cansuppress engodenous or extraneous oncogene C-myc transcription in transcriptionallevel. C-myc is the downstream target gene of the PI3K signal transduction pathway,when PTEN blocks the PI3K signal transduction pathway,C-myc gene expressionproduct production decreases, the PTEN protein apoptosis has close correlation withthe C-myc expression drops ,namely PTEN and C-mycassume the inversecorrelation. Both C-myc protein and PTEN protein are playing the vital role in theoccurrence and development of the gastric cancer ,but their biological effects areadverse. It is not completely elucidated about their relationship in gastric cancer. Thisstudy was designed to investigate the role of C-myc protein and PTEN protein in thepathogenesis of gastric cancer and their correlation.Methods: the expression of C-myc and PTEN protein was examined bystreptavidin-peroxidase conjugated method (SP) in 63 cases of gastric cancer.Results: The positive rates of PTEN protein were 55.4 %,and C-myc protein 74.2%in 63 cases of gastric cancer。The expression of C-myc protein was significantlycorrelated with infiltration degree (P<0.01),histological differentiation (P<0.05) ,clinic TNM staging (P<0.01) and lymph node metastasis (P<0.05) of the gastriccancer. The expression of PTEN was positively correlated with infiltration degree(P<0.01),histological differentiation (P<0.05) , clinic TNM staging (P<0.05) andlymph node metastasis (P<0.01) ofthe gastric cancer,too. PTEN was negativelycorrelated with C-myc in early and advanced gastric cancer,but not in all cases.Inearly and advanced gastric cancer, the rates of C-myc( +)PTEN( -) were0.00%(0/13),48% (24/50)(P<0.01), the rates of C-myc( -)PTEN( + ) Were84.6%(11/13), 25.0%(11/44)(P<0.01).With the progress of tumor in malignancy andclinic TNM staging, the positive rate of C-myc expression increased, while that ofPTEN protein decreased. The rates of C-myc( + )PTEN( -) were6.67%(1/15),37.2%(16/37),63.6%(7/11) in Well, Moderate and Poor differentiationrespectively(P<0.01). On the contrary, the rates of C-myc(-)PTEN(+) were66.7%(10/15), 24.3%(9/37) and 18.2%(2/11) from Well to Poordifferentiationrespectively (P<0.05). The rates of C-myc(+)PTEN(-) were 16.7% (2/12),23.8%(5/21),56.6% (17/30) in Ⅰ,Ⅱ,Ⅲ+Ⅳ stage respectively (P<0.05). The rates ofC-myc(-) PTEN(+) were 58.3%(7/12),52.4%(11/21),13.3%(4/30) from Ⅰ to Ⅲ+Ⅳ stage (P<0.01). In non-lymph node metastases and lymph node metastases cases,The rates of C-myc(+)PTEN(-) were 15.8%(3/19), 47.7%(21/44) (P<0.05). therates of C-myc(-)PTEN(+) were 63.2% (12/19) , 22.7%(10/44)(P<0.01).The ratiodemonstrated ascending tendency about C-myc and descending tendency aboutPTEN with the advancement of gastric cancer . There was a negative correlationbetween C-myc and PTEN in gastric cancer.Conclusions: C-myc was negatively correlated with C-myc in gastriccancer.Detection of C-myc together with PTEN is valuable for evaluating malignancyextent and prognosis of gastric cancer.