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Tristetraprolin posttranscriptionally down-regulates PFKFB3 in cancer cells

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Abstract
The enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases 3(PFKFB3) catalyzes the first committed rate-limiting step of glycolysis and is upregulated in cancer cells. The mechanism of PFKFB3 expression upregulation in cancer cells has not been fully elucidated. The PFKFB3 3’-UTR is reported to contain AU-rich elements(AREs) that are important for regulating PFKFB3 mRNA stability. However, the mechanisms by which PFKFB3 mRNA stability is determined by its 3’-UTR are not well known. We demonstrated that tristetraprolin(TTP), an ARE-binding protein, has a critical function regulating PFKFB3 mRNA stability. Our results showed that PFKFB3 mRNA contains three AREs in the 3’-UTR. TTP bound to the 3rd ARE and enhanced the decay of PFKFB3 mRNA. Overexpression of TTP decreased PFKFB3 expression and ATP levels but increased GSH level in cancer cells. Overexpression of PFKFB3 cDNA without the 3’-UTR rescued ATP level and GSH level in TTP overexpressing cells. Our results suggested that TTP post-transcriptionally downregulated PFKFB3 expression and that overexpression of TTP may contribute to suppression of glycolysis and energy production of cancer cells in part by downregulating PFKFB3 expression.
Author(s)
장지훈
Issued Date
2019
Awarded Date
2020-02
Type
Dissertation
URI
https://oak.ulsan.ac.kr/handle/2021.oak/6431
http://ulsan.dcollection.net/common/orgView/200000288647
Alternative Author(s)
Ji Hun Jang
Affiliation
울산대학교
Department
일반대학원 생명과학과
Advisor
박정우
Degree
Master
Publisher
울산대학교 일반대학원 생명과학과
Language
eng
Rights
울산대학교 논문은 저작권에 의해 보호받습니다.
Appears in Collections:
Life Science > 1. Theses (Master)
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