Journal
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
Volume 2022, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2022/8693259
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Funding
- National Natural Science Foundation of China [81702540]
- Natural Science Foundation of Anhui Province [1808085MH292, 2108085MH293]
- Key Research and Development Project of Anhui Province [202004J07020022]
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This study reveals that MALAT1 controls prostate cancer proliferation and glucose metabolism by upregulating the MYBL2-mTOR axis, and knocking down MALAT1 or MYBL2 significantly inhibits the proliferation capacity of PCa cell lines.
It is known that the long noncoding RNAs (lncRNA) MALAT1 is associated with tumorigenesis and progression in various cancers; however, its functions and mechanisms in prostate cancer (PCa) initiation and progression are still unknown. In the present study, our findings revealed that MALAT1 plays a critical part in regulating PCa proliferation and glucose metabolism. Knockdown of MALAT1 affects the protein and mRNA levels of MYBL2. In addition, MALAT1 enhances the phosphorylation level of mTOR pathway by upregulating MYBL2. Knockdown of MALAT1 or MYBL2 in PCa cell lines significantly inhibits their proliferation capacity. Silencing MALAT1/MYBL2/mTOR axis in PCa cell lines affects their glycolysis and lactate levels, and we verified these findings in mice. Furthermore, we explored the underlying tumorigenesis functions of MYBL2 in PCa and found that high expression of MYBL2 was positively associated with TNM stage, Gleason score, PSA level, and poor survival rate in PCa patients. Taken together, our research suggests that MALAT1 controls cancer glucose metabolism and progression by upregulating MYBL2-mTOR axis.
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