The Study Of The Gene Copy Number Variation In Cervical Cancer By Array Comparative Genomic Hybridization (ACGH)

Human papillomaviruses (HPV) infecton is the important but not only cause of cervical cancer. The gene variation resulted from HPV infection may be the most important reason to cervical cancer. So we use human whole genome array comparative genomic hybridization to detect the copy number variations of genes in cervical cancer. The result of the array is validated by PCR, FISH and immunohistochemisty. We find that the copy number and protein expression of CLDN1 increase with the progression of cervical cancer. The rate of strong positive expression of CLDN1 in the cervical cancer with lymph node metastasis is higher than that in the cancer without lymph node metastasis. Over-expression of CLDN1 in SIHA can promote the ability of migration and invasion accompanied with epithelial markers decrease and mesenchymal markers increase. And we also find that CLDN1 could enhance the ability of apoptosis resistance and colony formation in SIHA. The activity of MMP-9 is enhanced in SIHA with CLDN1 over-expression. The mechanism of CLDN1 related epithelial- mesenchymal transition (EMT) may be through the interaction between CLDN1 and SNAI1, SNAI2. EMT and associated apoptosis resistance, MMP activation and ability of survival may be the mechanism which promotes cervical cancer progression and metastasis. Our findings may supply the new evidence for clarifying the mechanism of cervical cancer progression and early diagnosis of cervical cancer.