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Investigating the Role of Ca2+ and the Acto-myosin Mechanism on the Human MCF-7 Breast Cancer Cell Line

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MLA citation style (9th ed.)

Scherer, Bri, and Bhetwal, Bhupal. Investigating the Role of Ca2+ and the Acto-myosin Mechanism On the Human Mcf-7 Breast Cancer Cell Line. . 1120. mushare.marian.edu/concern/generic_works/e1661e6c-a4c5-4a2c-ac70-f11c0294672c?locale=fr.

APA citation style (7th ed.)

S. Bri, & B. Bhupal. (1120). Investigating the Role of Ca2+ and the Acto-myosin Mechanism on the Human MCF-7 Breast Cancer Cell Line. https://mushare.marian.edu/concern/generic_works/e1661e6c-a4c5-4a2c-ac70-f11c0294672c?locale=fr

Chicago citation style (CMOS 17, author-date)

Scherer, Bri, and Bhetwal, Bhupal. Investigating the Role of Ca2+ and the Acto-Myosin Mechanism On the Human Mcf-7 Breast Cancer Cell Line. 1120. https://mushare.marian.edu/concern/generic_works/e1661e6c-a4c5-4a2c-ac70-f11c0294672c?locale=fr.

Note: These citations are programmatically generated and may be incomplete.

Cancer cells have shown to exhibit enhanced potential to metastasize via increased actin-myosin crossbridge formation, which requires increased Ca2+ influx via the voltage-gated calcium channels. This then leads to the activation of myosin light chain kinase (MLCK). MLCK then phosphorylates myosin light chain and forms the actin-myosin cross bridges Additionally, the PI3-Kinase/Akt pathway is critical for cell survival and division, which works from the activation of Akt through phosphorylation of PI,4,5BP by PI-3 kinase. These two critical cell survival pathways have been extensively studied in the field of breast cancer cell research and my research is primarily focused on investigating the role of VGCC, MLCK and PI-3 kinase on MCF-7 cell viability by using pharmacological inhibitors to assess significant changes in morphology and cell survival via microscopy and MTT assays.

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