ObjectiveBreast cancer is the leading cause of death of the primary tumor causedby disseminated widely, and extensive axillary lymph node metastasis isoften the basis for evaluation therefore become a lymph node metastasis ofbreast cancer prognosis and treatment of the main selection criteria. A largenumber of clinical trials showed that tumor cells migrate to the lymph nodesmust be lymphatics, newborn promotes tumor lymphatic lymph nodemetastasis, and vascular endothelial growth factor receptor3(VEGFR-3) isinduced lymphangiogenesis key protein, it by vascular endothelial growthfactor-C and D (VEGF-C and VEGF-D’s) activated for tumorlymphangiogenesis create favorable conditions. Phosphatidylinositol3-kinase/serine threonine protein kinase B (PI3K/AKT) signaling pathwayregulates tumor cell proliferation and apoptosis, in the vast majority ofhuman tumors expressing disorders, and participate in IGF-1-induced theupregulation of VEGF-C in breast cancer lymph node metastasis plays animportant role. But PI3K/AKT pathway in breast cancer lymph nodemetastasis mechanism of action is not entirely clear, the subject of researchin the literature, based on the detection of breast cancer through thePI3K/AKT pathway related genes to analyze its relationship withlymphangiogenesis related factors VEGFR-3, VEGF-C expression, toexplore the PI3K/Akt signaling pathway in breast cancer lymphangiogenesisrelations and further reveal the molecular basis of breast cancer lymph nodemetastasis mechanism for the treatment of breast cancer provide new ideas.Materials and methodsCollected in July2010-July2012Taishan Medical Hospital after surgical resection, after HE staining pathological diagnosis of invasiveductal carcinoma postoperative specimens, a total of30cases, including15cases with lymph node metastasis, no lymph node metastasis group of15cases. Reverse transcriptase polymerase chain reaction (RT-PCR) techniquecombined semi-quantitative detection of AKT-mRNA, PI3K mRNA,VGFR-3mRNA, VEGF-CmRNA in the case of breast cancer tissues. Thenwe used SPSS13.0software to analyze their relationships and correlationswith clinicopathologic findings.Results(1)30cases of breast cancer fresh specimens, PI3KmRNA lymph nodemetastasis in invasive ductal carcinoma relative expression levels(0.661±0.202) were higher than those without lymph node metastasis group(0.226±0.193), the difference between the two groups was statisticallysignificant, t=-5.470p <0.05.(2)30cases of breast cancer fresh specimens, AKTmRNA lymph nodemetastasis in invasive ductal carcinoma relative expression levels(0.645±0.189) were higher than those without lymph node metastasis group(0.245±0.169), the difference between the two groups was statisticallysignificant, t=-6.093p <0.05.(3) PI3KmRNA relative expression levels of VEGF-CmRNA withrelative expression levels by linear correlation analysis, the correlation inbreast cancer correlation coefficient r=0.477, p=0.008(p <0.05), werepositively correlated. PI3KmRNA relative expression levels (0.455±0.259)and VEGFR-3mRNA relative expression level (0.413±0.229), the linearcorrelation analysis, the correlation coefficient in breast cancer r=0.580, p=0.001(p <0.05), were positively related.(4) AKTmRNA relative expression levels of VEGF-CmRNA withrelative expression levels by linear correlation analysis, the correlationcoefficient in breast cancer r=0.708, p=0.000(p <0.05), were positivelycorrelated. AKTmRNA relative expression levels (0.455±0.247) andVEGFR-3mRNA relative expression level (0.413±0.229), the linearcorrelation analysis, the correlation coefficient in breast cancer r=0.391, p=0.013(p <0.05), were positively related.Conclusions (1) PI3KmRNA, AKTmRNA with lymph node metastasis of breastcancer with high expression, suggesting that PI3K gene expression andlymph node metastasis was significantly correlated.(2) PI3KmRNA with VEGF-CmRNA, VEGFR-3mRNA in breast cancertissues were positively correlated, suggesting that PI3K may increaseVEGF-C, VEGFR-3expression in breast cancer, and throughVEGF-C/VEGFR-3signaling system, and thus play its inhibition oflymphatic endothelial cell apoptosis, and promote the role oflymphangiogenesis.(3) AKTmRNA with VEGF-CmRNA, VEGFR-3mRNA in breast cancertissues were positively correlated, AKT may contribute to VEGF-C,VEGFR-3expression in breast cancer, but also signaling pathways throughVEGF-C/VEGFR-3, lymphangiogenesis of breast cancer.(4) VEGF-C, D/VEGFR-3and PI3K/AKT signaling pathways may existcross-dialogue, which play on the overall regulation of lymphangiogenesisrole in promoting breast cancer lymphangiogenesis. |