AFALC · Analyzing the functions of AP-1 in liver carcinogenesis
6РП — Действия „Мария Кюри“
- Период
- 2005-10-15 → 2007-10-14
- Финансиране от ЕС
- 158 454 €
- Участници
- 1
- Схема
- IIF
Линиите свързват координатора с партньорите. За проекти отпреди 2014 г. CORDIS не винаги дава точни координати. Тези точки са на ниво град или държава.
Накратко на български
Протеините JNK и c-Jun влияят върху развитието на рака на черния дроб, като например c-Jun помага за оцеляването на раковите клетки. Разбирането на тези механизми помага при търсенето на нови методи за терапия срещу това заболяване.
Кратко обяснение, генерирано от езиков модел по текста на CORDIS. Оригиналът е по-долу.
Резултати накратко
Final Activity Report Summary - AFALC (Analysing the functions of AP-1 in liver carcinogenesis)
I have been studying the roles of MAPKs (p38alpha and JNK1/2) and AP-1 (c-Jun and c-Fos) in liver cancer development. Using a chemical-induced cancer model, I found that p38alpha suppresses proliferation of cancer cells by antagonising the JNK/c-Jun pathway. On the other hand, JNK1, but not JNK2, is essential for mouse liver cancer development. In addition, my results also showed that c-Jun promotes survival of initiated liver cancer cells by repressing c-Fos expression. Taken together, my data strongly indicate that the JNK/c-Jun pathway is a valuable target for liver cancer therapy.
Текст от CORDIS, на английски · Данни: CORDIS, © Европейски съюз
Цел на проекта
Hepatocellular carcinoma (HCC) causes about 500,000 deaths worldwide each year and is the leading cause of cancer mortality in some parts of the world. Although the pathogens for HOC are quite clear, the molecular mechanisms through which they induce HOC development still need to be clarified. AP-1 genes encode transcription factors, which possibly play important roles in many cancers, including HOC.Until now, little is known about their functions in liver carcinogenesis. In this respect, I will investigate AP-1 functions in genotoxiccarcinogen induced HCC using conditional knock-out mice. This study will focus on c-Jun, c-Fos and p53pathways and their interactive functions in liver cancer, especially in the early stages of carcinogenesis. Molecules responsible f or dysregulated apoptosis and proliferation will be identified by molecular, immunohistological and micro-array analyses.This project will uncover novel insights into the molecular mechanisms involved in HCC, which may provide new avenues for the development of diagnostic and drug targets in the future.
Оригинален текст от CORDIS (на английски).
Участници
- RESEARCH INSTITUTE FOR MOLECULAR PATHOLOGY · VIENNAКоординаторНиво градАвстрия
Връзки
Данни: CORDIS, © Европейски съюз