碩士 / 國立臺灣師範大學 / 生命科學系 / 106 / I
Thyroid receptor interacting protein 6（TRIP6）is a downstream signaling molecule of lysophosphatidic acid（LPA）receptor. It enhances activation of signaling molecules regulating actin to induce cell migration, division and proliferation. TRIP6 is overexpressed in glioblastoma multiform（GBM）and may be a characteristic of aggressiveness of GBM. Interferon induced protein with tetratricopeptide repeats 5（IFIT5）is a member in interferon induced protein family, and involves in the regulation of human innate immune response. It has been reported that IFIT5 interaction with actin on the cell cortex, and may involve in the regulation of cell migration. To examine whether IFIT5 plays a role in the TRIP6 regulated cell migration and glioblastoma tumorigenesis, we investigated the interaction of these two proteins. Here, we demonstrated the interaction of IFIT5 and TRIP6 in cells by co-immunoprecipitation. Moreover, we elucidated the effect of these two proteins on cell migration by live cell imaging, and found that IFIT-5 itself does not enhance the cell blebbing, but promotes TRIP6-mediated cell dynamics.
II
Glioblastoma multiforme （GBM）, classified as the grade IV astrocytoma, is the most common malignant brain cancer in adult. GBM possess the characters of invasiveness, heterogeneity and resistance to chemical and radiation therapy. The GBM patients have poor prognosis, the median survival of the patients is about 14 months. Some studies have showed that the glioblastoma stem cells（GSCs）, a small population of cells, may play the critical role in cancer relapse. Therefore, targeting GSCs is one of the potential therapeutic strategies for GBM. Recent researches studied the plant extracts and found the anti-inflammatory, anti-virus and anti-cancer activity of compositions in the plants. These components can be developed further to other structurally similar molecules for treatment of diseases. In this study, we detection that two extracts and neriifolin inhibited viability and movement of GBM cells and GSCs, and induced cell cycle arrest and apoptosis of GSCs. Stimulation of GSCs with neriifolin inhibited activity of Akt pathway to reduce cell viability and maintain of GSCs.
| Identifer | oai:union.ndltd.org:TW/106NTNU5112033 |
| Creators | Liu, Wen-Shan, 劉文善 |
| Contributors | Lai, Yun-Ju, 賴韻如 |
| Source Sets | National Digital Library of Theses and Dissertations in Taiwan |
| Language | zh-TW |
| Detected Language | English |
| Type | 學位論文 ; thesis |
| Format | 67 |
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