Research On Sam68Promote Invasion And Metastasis Of Breast Cancer Cells

Breast cancer is one of the most common malignancies impact on women’shealth and even life-threatening, ranking second in female cancer incidence andincidence dropping year by year, to become the disease that serious harm to women’shealth. Most breast cancer deaths because invasion and metastasis of cancer cell,about50%of the reported early breast cancer had lymphatic metastasis, and axillarylymph nodes is the most common site of breast cancer metastasis, and is the onlymetastatic lymph node for a very long time.Or without axillary lymph nodemetastasis is an important factor in breast cancer recurrence and metastasis. Therefore,search effectively biomarkers that predict lymph node metastasis are particularlyimportant for the choice of clinical treatment programs，which will provide newmolecular markers and targets in the diagnosis and prediction of breast cancer.The key event of early metastasis-Epithelial-to-mesenchymal transition (EMT)plays an important role in metastasis, regardless of invasion or infiltration of cancercells are dependent on obtaining EMT characteristics. Scientists have also found EMTsign is characterized by loss of expression of E-cad protein，the loss of E-cadexpression may increase tumor cell invasion have been shown in vitro experiments,the expression levels of E-cad has been used as one of the hallmarks of tumormetastasis. Currently known Snail, Slug, Twist, SIP-1, ZEB-1transcription factor and E12/E47can act directly on the E-cad promoter, reduced the expression of E-cad andresulted in EMT phenomenon.1994Fumagalli S and his partners found sam68protein (Src-associatedsubstrated during mitosis of68KD), found that sam68upregulated in most tumors,theexpression level was significantly related with clinicopathological factors andprognosis，our previous studies have confirmed the higher Sam68expression rate，themore lymph node metastasis，then patients with worse prognosis. We also found that:Sam68protein was negatively correlated with E-cadherin expression level, suggestingthat Sam68possible induced EMT events by regulating E-cadherin and then promotebreast cancer lymph node metastasis, this part of study is less both at and abroad.Thestudy about sam68protein effect and mechanisms on EMT and infiltration of breastcancer cell may be provide a new target for the treatment of breast cancer, which hasbecome a new hotspot.Objective: To investigate the sam68expression impact on EMT and itsmechanism in breast cancer cells.Methods: High invasiveness MBA-MD-231cells with mesenchymalcharacteristics and low invasiveness MCF-7cells with the characteristics of epithelialtissue by RT-PCR and WB to detect the sam68expression levels of both cells. Designthree kinds of siRNA fragments targeted sam68, liposome-mediated transfectiontransform them into breast cancer cells. By real-time PCR and wersten blot detectionmeans to pick out the most efficient siRNA fragments that silence sam68. SelectedsiRNA fragments interfer with breast cancer cells, then compare E-cadherin levels andinvasive ability with normal cancer cells. Application of statistical software SPSS13.0to analysis.Results:(1) After siRNA interference，expression of sam68protein significantly reducedin MBA-MD-231cells, expression of E-cadherin protein is up-regulated,that meansEMT is inhibited.(2) After siRNA interference,migration and invasion of cancer cells decreasedsignificantly. Conclusion: After the sam68gene interferenced by siRNA technology canInhibit the EMT of breast cancer cell, and thus reduced the ability of migration andinvasion.