RAC1 in keratinocytes regulates crosstalk to immune cells by Arp2/3-dependent control of STAT1.

Rac 1 function in skin inflammation 1 RAC 1 in keratinocytes regulates crosstalk to immune cells by Arp 2 / 3 dependent control of STAT 1

Crosstalk between Tumor Cells and Immune System Leads to Epithelial-Mesenchymal Transition Induction and Breast Cancer Progression

Herein, we review the current findings of how a variety of accessory cells could participate in shaping the tumor microenvironment and supporting the mechanisms by which cancer cells undertake the epithelial-mesenchymal transition (EMT). EMT, a complex of phenotypic changes, promotes cancer cell invasion and creates resistance to chemotherapies. Among the accessory cells present in the EMT, imm...

بررسی اثر ملیتین بر میزان بیان پروتئین Rac1 به عنوان مارکر متاستاز در سلول‌های سرطان معده رده AGS

Introduction: Understanding the molecular mechanisms of metastasis is important for the design and effective use of novel therapeutic strategies in order to combat metastases. One class of molecules that has been implicated in metastasis is Rac1. Regarding complications of conventional therapies such as chemotherapy, current studies are evaluating natural compounds with anticancer Properties. M...

Rac1 regulates skin tumors by regulation of keratin 17 through recruitment and interaction with CD11b+Gr1+ cells

Rac1 is a member of the Rho family of small GTPases that control cells proliferation, differentiation, migration, and inflammation. Rac1 is crucial in tumorigenesis and development. Keratin17 and CD11b+Gr1+ cells are considered to regulate skin inflmmation. Here we discuss the regulation of Rac1 on skin tumor formation and its relationship. In samples from human skin squamous cell carcinoma (SC...

RAC1 activation drives pathologic interactions between the epidermis and immune cells.

Interactions between the epidermis and the immune system govern epidermal tissue homeostasis. These epidermis-immune interactions are altered in the inflammatory disease psoriasis; however, the pathways that underlie this aberrant immune response are not well understood. Here, we determined that Ras-related C3 botulinum toxin substrate 1 (RAC1) is a key mediator of epidermal dysfunction. RAC1 a...