Journal Article DKFZ-2018-00237

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miR-137 inhibits melanoma cell proliferation through downregulation of GLO1.

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2018
Springer37831 Heidelberg

Science in China / C 61(5), 541-549 () [10.1007/s11427-017-9138-9]
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Abstract: Late-stage melanoma is refractory to current therapies. MicroRNAs (miRNAs) can modulate many physiological and pathological processes of melanoma. Studies have demonstrated that miR-137 acts as a tumor suppressor by inhibiting the proliferation of melanoma cells through targeting multiple mRNAs. The glyoxalase system member glyoxalase 1 (GLO1) is the principal scavenging enzyme of methylglyoxal (MG), a toxic byproduct of glycolysis. Using35S in vivo/vitro labelling analysis for dynamic proteomics (SiLAD), we found that miR-137 downregulated the expression of GLO1 in melanoma cells. Bioinformatics analysis predicted that GLO1 is a direct target of miR-137. This was validated by dual luciferase reporter assay. Quantitative RT-PCR (qRT-PCR) and western blot analysis indicated that miR-137 could decrease endogenous GLO1 expression. Furthermore, siRNA targeting of GLO1 mimicked inhibition of melanoma cell proliferation caused by miR-137 overexpression. Re-expression of GLO1 was able to restore miR-137-mediated suppression of melanoma cell proliferation. Therefore, these results suggest that miR-137 inhibits the proliferation of melanoma cells by targeting GLO1.

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Note: 2018 May;61(5):541-549

Contributing Institute(s):
  1. GMP Einheit Zelluläre Therapie (G182)
Research Program(s):
  1. 317 - Translational cancer research (POF3-317) (POF3-317)

Appears in the scientific report 2018
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Medline ; Creative Commons Attribution CC BY (No Version) ; DOAJ ; Allianz-Lizenz / DFG ; BIOSIS Previews ; Current Contents - Life Sciences ; DOAJ Seal ; IF < 5 ; JCR ; NCBI Molecular Biology Database ; NationallizenzNationallizenz ; SCOPUS ; Science Citation Index ; Science Citation Index Expanded ; Thomson Reuters Master Journal List ; Web of Science Core Collection ; Zoological Record
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 Record created 2018-03-07, last modified 2024-02-29



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