KLI

The role of ADAR1 in the Mobility and Metabolic adaptation

Metadata Downloads
Abstract
RNA editing is a well-known post-transcriptional event and deamination is one of the major processes. There are two types of deamination of RNA: cytidine to uridine and adenosine to inosine. The A-to-I transition is edited by ADAR1 (Adenosine Deaminase, RNA Acting on RNA), which recognizes double-stranded RNA. A to I RNA deamination occurs primarily at the Alu repeats and functionally at the 3'UTR region, coding sequence, and microRNA precursors. This can result in recoding of a target gene or alter its expression and function. Recent studies suggested the novel role of ADAR1 in the treatment of human cancers, including epigenetic therapy and immunotherapy. We aimed to find out the role of ADAR1 in human breast cancer cells by combined analysis of RNA seq and cellular analysis after ADAR1 depletion. As a result, we found the depletion of ADAR1 suppresses the expression of ARPIN in an editing-independent manner. As the ARPIN inhibits the branching of actin filaments, the ADAR1 depletion stimulated cell mobility. On the other hand, we revealed the role of ADAR1 in the glucose-limiting condition. Specifically, when ADAR1 was depleted, we found an enhanced autophagic response and increased viability of breast cancer cells. This response seems to be triggered by activated AMPK that subsequently activated Beclin-1 and LC3. Altogether, these results present a new role of ADAR1 in breast cancer.
Author(s)
박민지
Issued Date
2022
Awarded Date
2022-02
Type
dissertation
Keyword
ADAR1Breast cancerRNA editing
URI
https://oak.ulsan.ac.kr/handle/2021.oak/10013
http://ulsan.dcollection.net/common/orgView/200000605399
Alternative Author(s)
Park Min Ji
Affiliation
울산대학교
Department
일반대학원 의학과의과학전공
Advisor
장수환
Degree
Doctor
Publisher
울산대학교 일반대학원 의학과의과학전공
Language
eng
Rights
울산대학교 논문은 저작권에 의해 보호 받습니다.
Appears in Collections:
Medical Science > 2. Theses (Ph.D)
Authorize & License
  • Authorize공개
Files in This Item:

Items in Repository are protected by copyright, with all rights reserved, unless otherwise indicated.