Cartel de Metodología de Investigación, Resúmenes de Investigación Comercial

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1D 3934 mr p21-Activated Kinase 1 Promotes Breast Tumorigenesis LI F IZTACALA via Phosphorylation and Activation of the Calcium/Calmodulin-Dependent Protein Kinase ll. INVESTIGACIÓN E omisión DE Es INVESTIGACIÓN Y "2 poscrapo SALDIVAR CERON HECTOR IVAN *2, VILLAMAR CRUZ OLGA *, HERNANDEZ RIVAS ROSAURA *. ARIAS ROMERO LUIS ENRIQUE * 1 Carra de Malo Cirujano, Facultas de Estuss Supero Itaca, Universia Naciona Autinoma de Ménico, Tisinepanti 54090, México 2. Laberatoo 14, Unidas de Bromestina (USED), Facutad ce Estudos Supenares Ixtseala, Universos Nacional Autónsma de Méxio, Tlaepantia 54000, Miér 3 Departamento de Blomadena Molecular Centro de Investigación y de Estudis Supercres (ONVESTAVIPN). Uria Zacatenco INTRODUCTION. Breast cancer, one of the leading causes of cancer-related deaths in women, presents in several subtypes, including Luminal A and B, Her2+, and Triple Negative Breast Cancer (TNBC). Each subtype is primarily characterized by varying receptor expression levels and differing responses to treatment. Signal transduction, especially involving the phosphoinositide 3-kinase (PISK/AkUmTOR, Ras/RAF/MEK/ERK, and Src/Fak pathways, plays a crucial role in cancer progression. The p21 activated kinase, Pak1, has been identified as a key player in these networks. However, the role of Pak1 in tumorigenesis A remains not fully understood. In our study, we delve into the role of Pak1 and its interaction with the Calcium/Calmodulin-Dependent raro Protein Kinase || (CalMKII) in breast cancer cells. We find that Pak1 and CaMKIl expression correlates in breast “"* cancer cell lines and impacts cell proliferation, migration, —..,,., On and invasion. These findings provide insight into potential therapeutic targets for the effective treatment of TNBC. FIGURES. Pakand CalK! pharmacologicalInhibiionreduces cell prolferation and induces apoptosis in breastcancer cells 30 cultures. FIGURE4, Synergistic interactions between Pak and GalAKIl Inhibitoss. MGET SK-BRI MDA-MB-231 Aci ln Huctel PENA, Merge _Aclin Nuciel PENA Vehicte e us RESULTS. PLES FIGURES. breast can A _o A FIGURE2, Pak interacts with GaMKIlin a cellular context. e S cuna 4 FIGURET, Inhibitionof Pak and Call impedes the tumorigenicity of triple negative breastcancer cells MDA-M8.231 cells were injected into the flanks of BALB!c-nunu mice. Conclusion. Our research highlights the novel interaction between Pak1 and CaMKII in : s breast cancer cells. Inhibition of both led to decreased invasiveness in FIGURES. Correlatino! Immunohistochemicalsalning of Pak and Call In human bresstcancer TNBC cells and tumor growth delay. This suggests a potential therapeutic strategy for treating TNBC.