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[ subject:"Cellular biology." ]
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Silencing Egr1 radioprotects normal ...
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Zhao, Diana Yi.
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Silencing Egr1 radioprotects normal tissues while potentiating the effects of radiation on cancer cells.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Silencing Egr1 radioprotects normal tissues while potentiating the effects of radiation on cancer cells./
作者:
Zhao, Diana Yi.
出版者:
Ann Arbor : ProQuest Dissertations & Theses, : 2017,
面頁冊數:
100 p.
附註:
Source: Dissertation Abstracts International, Volume: 78-08(E), Section: B.
Contained By:
Dissertation Abstracts International78-08B(E).
標題:
Cellular biology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10259836
ISBN:
9781369651539
Silencing Egr1 radioprotects normal tissues while potentiating the effects of radiation on cancer cells.
Zhao, Diana Yi.
Silencing Egr1 radioprotects normal tissues while potentiating the effects of radiation on cancer cells.
- Ann Arbor : ProQuest Dissertations & Theses, 2017 - 100 p.
Source: Dissertation Abstracts International, Volume: 78-08(E), Section: B.
Thesis (Ph.D.)--Washington University in St. Louis, 2017.
Radiation therapy utilizes ionizing radiation (IR) to destroy cancer cells, but unintended damage to the surrounding normal tissue results in both short and long term side effects that reduce quality of life. In order to improve the therapeutic index of radiotherapy, we are interested in blocking radiation damage to normal tissues and/or enhancing the anti-cancer effects of radiation. Apoptosis is a key element of the radiation response in normal tissues that contributes to tissue injury. Thus, we targeted a regulator of radiation-induced apoptosis---the Early Growth Response 1 (Egr1) transcription factor, which activates the transcription of pro-apoptotic genes in response to IR. We demonstrate that the genetic abrogation of Egr1 attenuates radiation-induced apoptosis in normal tissues in an Egr1 knockout mouse model and in normal cell culture models. These events correlate with an abrogation of p53 induction by IR.
ISBN: 9781369651539Subjects--Topical Terms:
3172791
Cellular biology.
Silencing Egr1 radioprotects normal tissues while potentiating the effects of radiation on cancer cells.
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Radiation therapy utilizes ionizing radiation (IR) to destroy cancer cells, but unintended damage to the surrounding normal tissue results in both short and long term side effects that reduce quality of life. In order to improve the therapeutic index of radiotherapy, we are interested in blocking radiation damage to normal tissues and/or enhancing the anti-cancer effects of radiation. Apoptosis is a key element of the radiation response in normal tissues that contributes to tissue injury. Thus, we targeted a regulator of radiation-induced apoptosis---the Early Growth Response 1 (Egr1) transcription factor, which activates the transcription of pro-apoptotic genes in response to IR. We demonstrate that the genetic abrogation of Egr1 attenuates radiation-induced apoptosis in normal tissues in an Egr1 knockout mouse model and in normal cell culture models. These events correlate with an abrogation of p53 induction by IR.
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Additionally, we study whether the radioprotection conferred by Egr1 silencing is selective to normal cells or if it would also impair the cytotoxic effects of IR on cancer cells. A clinically useful molecular target for radioprotection should ideally provide selective protection to normal cells but exclude cancer cells from the protective effects. To study whether targeting Egr1 radioprotects cancer cells, we genetically abrogated Egr1 in several cancer cell lines that represent tumors that typically undergo radiation treatment and are associated with adverse normal tissue side effects. Targeting Egr1 in these cancer cells actually decreases their growth and survival and has an additive effect on the efficacy of IR. These effects are associated with decreased survival signaling through the AKT-mTOR pathway.
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In summary, targeting Egr1 uniquely produces differential effects on normal tissues and cancer cells. These data support the potential of silencing Egr1 in order to minimize the normal tissue complications associated with radiotherapy while enhancing tumor control. Exploiting the paradoxical function of Egr1 in normal versus cancer cells could help improve the therapeutic index of radiotherapy.
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