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However, the function of Annexin A2 in ovarian cancer progression remains unclear. In this study, we aimed to investigate the role and underlying molecular mechanism of Annexin A2 in cell proliferation and invasion in ovarian cancer.
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We found that the mRNA expression of Annexin A2 was upregulated in ovarian cancer tissues and cell lines. In the loss-of-function of Annexin A2, β-catenin was indicated to be significantly suppressed and EMT constrained.
Moreover, cell proliferation and invasion were both markedly inhibited by the downregulation of Ovarian cancer treatment options. Additionally, the overexpression of β-catenin obviously reversed the effect of Annexin A2 on EMT, and cell proliferation and invasion, indicating that Annexin A2 suppression regulated EMT through controlling β-catenin.
Introduction Ovarian cancer ranks among the most lethal of gynecological malignancies 1 — 3. In addition, ovarian cancer has a low 5-year survival rate 15.
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Invasion and proliferation are the significant attributes of malignant cancer that result in high mortality in ovarian cancer. Thus far, the underlying molecular mechanism of ovarian cancer remains unclear.
A better understanding of the underlying mechanism of the invasion and proliferation in ovarian cancer could provide novel insights for the treatment of ovarian cancer. Annexin A2 is present in human endothelial cells, monocytes, macrophages, neuron, and some tumor cells 810 — The transformed cells ovarian cancer treatment options high levels of Annexin A2, and the terminally differentiated cells have low expression of Annexin A2 In the cells of tumors such as breast, liver, prostate and gastric cancers, Annexin A2 has been reported to be upregulated 14 — It is indicated that Annexin A2 is closely related to cell migration, invasion and adhesion in cancers 817 Studies have demonstrated that Annexin A2 promoted invasion of tumor cells containing glioma cells, and human hepatocellular carcinoma cells 8 Additionally, it is reported that Annexin A2 accelerated proliferation and invasion of human breast cancer SK-BR-3 cells Annexin A2 is indicated to be a predictor of serous ovarian cancer outcome and accelerates ovarian cancer metastasis However, the underlying mechanism of Annexin A2 in cell invasion and proliferation in ovarian cancer ovarian cancer treatment options yet to be elucidated.
The abnormal function and regulation of β-catenin could lead to aberrant activation of the Wnt signaling pathway, resulting in abnormalities of gene expression, cell adhesion, and cancer progression Additionally, studies have reported that β-catenin is closely related to tumorigenesis 23 In normal cells, there is only a small amount of free intracellular β-catenin and it cannot enter the ovarian cancer treatment options nucleus to regulate gene expression.
Many studies have shown that β-catenin is upregulated in many cancers and is associated with poor prognosis The upregulation of β-catenin induces cell proliferation and invasion in cancers such as ovarian cancer, breast cancer, colorectal cancer, and gastric carcinoma 26 — It has been shown that β-catenin has an effect on the regulation of EMT Epithelial-mesenchymal transition EMT is demonstrated to be a process whereby epithelial cells change to mesenchymal cells with decreased E-cadherin and increased N-cadherin E-cadherin is the adhesion molecule of epithelial cell surface, and plays an important role in the adhesion between cells The downregulation of E-cadherin is an important feature of EMT Additionally, EMT is a significant cause of tumor ovarian cancer treatment options and metastasis.
Studies have demonstrated that EMT induced cell invasion and proliferation in various cancers such as prostate cancer, breast ovarian cancer treatment options, colon cancer, and lung cancer 35 Moreover, EMT has been claimed to be induced and promote the cell invasion and proliferation in ovarian cancer 37 In this study, ovarian ovarian cancer treatment options treatment options focused on identifying the molecular mechanism of Annexin A2 in cell invasion and proliferation in ovarian cancer.
We investigated the expression of Annexin A2 in ovarian cancer treatment options cancer tissues and cell lines and revealed the effect of Annexin A2 inhibition on cell invasion and proliferation in ovarian cancer.
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Annexin A2 may thus be a promising molecular target for the treatment of ovarian cancer. This research was approved by the ethics committee at the Third Affiliated Hospital of Zhengzhou University.
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GAPDH was the internal reference gene. The membrane was washed with TBS before incubating with horseradish peroxidase conjugated secondary antibody Cell Signaling Technology.
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Finally, blots were analyzed in the Bio-Rad ChemiDoc apparatus. The relative protein expression was detected using Image-Pro Plus 6. The β-catenin fragment was ovarian cancer treatment options inserted into the plasmid pcDNA.
Next, the recombinant plasmids were transfected into E. Then, the amplified recombinant plasmids were extracted hpv uomo dopo quanto si manifesta by sequencing, and the correct plasmids were designated pcDNA.
Briefly, the cells were plated in the well plate followed by reaction 1 h with 10 µl of BrdU solution per well.
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Thereafter, a total of µl denaturing solution was added per well and reacted for 25 min. Cells were then stained with anti-BrdU antibody for 1. Finally, the results were detected at nm using a SpectroFluor Plus multiwell plate reader Tecan.