Cross talk between cancer immunity cycle and EMT; new light for study cancer progression
- سال انتشار: 1400
- محل انتشار: اولین همایش بین المللی و دهمین همایش ملی بیوانفورماتیک ایران
- کد COI اختصاصی: IBIS10_058
- زبان مقاله: انگلیسی
- تعداد مشاهده: 167
نویسندگان
Department of Pharmaceutical Biotechnology, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
Department of Pharmaceutical Biotechnology, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
Department of Pharmaceutical Biotechnology, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
چکیده
The immune system becomes involved in a complex set of interactions with different tumor cells. Severalsequential actions must be initiated and allowed to proceed and repeatedly expand for an anticancer immuneresponse to lead to the efficient destruction of cancer cells. These processes are known as the cancer Immunitycycle. On the other hand, epithelial to mesenchymal transmission (EMT) is another significant processinvolved in the development and invasion of cancer. Several similar pathways that regulate EMT are involvedin tumor-immune interactions, but little is known about the mechanisms and consequences of interferencebetween these regulatory processes. We performed comprehensive multi-omics analyses to determine theinterference between EMT and cancer immunity cycle and their clinical relevance in breast cancer. Weobtained relevant multi-omics data containing expression profiles, RNA sequencing data, and clinical datafrom ۱۱۱۹ breast cancer patients (BRCA, n = ۱۱۱۹) from The Cancer Genome Atlas (TCGA; tcgadata.nci.nih.gov/tcga). The EMT score of cancer cells was measured using the EMT signature, whichcompares the expression of epithelial marker genes and mesenchymal marker genes. We used two onlineservers (immune land escape and TIP) for the immune system status and merged these data. Our studydemonstrated the existence of complex and dynamic interaction between the cancer immunity cycle and EMTand their effect on cancer prognosis and treatment. Our study highlights the potential for EMT-immuneinterference as a model for explaining the underlying molecular mechanisms of cancer progression andguiding more effective and generalized cancer.کلیدواژه ها
Epithelial to mesenchymal transmission, Cancer immunity cycle, Omicsمقالات مرتبط جدید
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