Studies on Focal Adhesion Kinase in Human Breast Cancer Tissue
Autor: | Jaydip Biswas, Triparna Sen, Syamsundar Mandal, Kirat Kumar Ganguly, Amitava Chatterjee |
---|---|
Rok vydání: | 2012 |
Předmět: |
Oncology
medicine.medical_specialty medicine.diagnostic_test business.industry Cancer medicine.disease Focal adhesion Breast cancer Western blot Downregulation and upregulation Internal medicine Medicine Phosphorylation Immunohistochemistry RNA extraction biological phenomena cell phenomena and immunity skin and connective tissue diseases business |
Zdroj: | Journal of Cancer Therapy. :7-19 |
ISSN: | 2151-1942 2151-1934 |
DOI: | 10.4236/jct.2012.31002 |
Popis: | Aim: To study Expression and Phosphorylation status of Focal Adhesion Kinase (FAK) in Human Breast Cancer tissue. To study the relation of FAK with standard clinicopathological parameters of Human Breast Cancer. Methods: Tissue collection, Protein extraction, RNA isolation, Western Blot, Immunohistochemistry, RT-PCR, ELISA, Statistical analysis. Results: All the four techniques showed upregulated expression, phosphorylation (Tyr-397) and processing of FAK in human breast cancer tissue compared to the adjacent non-tumor tissue of the same patient. Upregulation of FAK was found to be increased parallely with the advancement of cancer. Localisation of FAK was found to be membrano-cytoplasmic. FAK is upregulated both in protein and mRNA level. Expression and phosphorylation of FAK is increased specifically in the tumor regions compared to the surrounding non-tumor region. Upregulation of FAK was frequently found in ER-positive and PR-positive but Her2/neu-negative breast cancer cases. Conclusion: FAK has crucial role in development and progression of human breast cancer. FAK may be considered as an indicator of human breast cancer progression. FAK processing may be considered as an indicator of invasive potential of breast cancer. FAK may be considered as a clinical indicator of human breast cancer development and progression. |
Databáze: | OpenAIRE |
Externí odkaz: |