期刊
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
卷 44, 期 6, 页码 2189-2200出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/ijmm.2019.4385
关键词
glutamine; proliferation; urinary bladder neoplasms; signal transducer and activator of transcription 3; reactive oxygen species; adenosine triphosphate; therapy
资金
- National Natural Science Foundation of China [81772713, 81472411, 81372752, 81401899]
- Taishan Scholar Program of Shandong Province [tsqn20161077]
- Natural Science Foundation [ZR2014HM088]
- Key Research and Development Program of Shandong Province [2018GSF118197]
- China Postdoctoral Science Foundation [2017M622144]
- Qingdao Postdoctoral Application Research Project
- Qingdao Young Scientist Applied Basic Research Fund [15-9-1-105-jch, 15-9-1-51-jch]
Changes in metabolism are common phenomena in tumors. Glutamine (Gln) has been documented to play a critical role in tumor growth. In this study, we aimed to to explore the mechanisms through which bladder cancer cells utilize Gln to fulfill their biosynthetic needs during proliferation. In addition, the roles of Gln in the tricarboxylic acid (TCA) cycle, reactive oxygen species (ROS) regulation, and signal transducer and activator of transcription 3 (STAT3) expression were examined in vitro in the T24 bladder cancer cell line. The results revealed that the T24 cell line was markedly Gln-dependent and that Gln supplementation promoted T24 proliferation through the actions of Gln as a ROS moderator and as a metabolic fuel in the TCA cycle. Importantly, extracellular Gln deprivation deregulated the production of the transcription factor, STAT3. Additionally, STAT3 expression was affected by the degree of Gln metabolism, as regulated by Gln intermediates and ROS. Thus, on the whole, the findings of this study demonstrate that Gln promotes the proliferation of the Gln-dependent bladder cancer cell line, T24, by supplementing adenosine triphosphate (ATP) production and neutralizing ROS to activate the STAT3 pathway.
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