Lnc<scp>RNA</scp>‐<scp>MIF</scp>, a c‐Myc‐activated long non‐coding <scp>RNA</scp>, suppresses glycolysis by promoting Fbxw7‐mediated c‐Myc degradation

Zhang, Pengfei; Cao, Limian; Fan, Pingsheng; Mei, Yide; Wu, Mian

doi:10.15252/embr.201642067

Cited by 96 publications

(65 citation statements)

References 52 publications

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“…This assay was conducted as previously reported (Zhang et al, 2016). Biotin-labeled sense or antisense oligos of LINC00202 were incubated with Y79 cell lysate for 1 h. The complex was pull down by streptavidin-coupled agarose beads (Invitrogen).…”

Section: Biotin Rna Pull-down Assaymentioning

confidence: 99%

Long Noncoding RNA LINC00202 Promotes Tumor Progression by Sponging miR-3619-5p in Retinoblastoma

Yan

et al. 2019

Cell Struct. Funct.

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Retinoblastoma (RB) is the most common intraocular malignancy in childhood, and the prognosis in the advanced RB is poor. It is urgent to find novel therapeutic targets. Long noncoding RNAs (lncRNAs) have critical functions in cancer progression, and lncRNA LINC00202 is found associated with poor prognosis in RB. However, the functions of LINC00202 in RB remain unclear. We employed qRT-PCR and immunoblot to detect the expression levels of mRNAs and proteins, respectively. Cell proliferation was determined by CCK-8 assay and colony formation assay. Transwell assays were applied to evaluate the cell abilities of migration and invasion. Luciferase reporter assay was applied to examine RNA stability, and RNA pulldown assays were used to detect interaction between lncRNA and microRNA (miRNA). LINC00202 expression in RB tissues is higher than that in the paired adjacent normal tissues, which has correlation with poor prognosis in RB. RB cell proliferation, migration and invasion were weakened by LINC00202 depletion, but enhanced by LINC00202 overexpression. MiR-3619-5p was identified to directly bind and mediate LINC00202-promoted RB progression, meanwhile, miR-3619-5p directly regulated expression of an oncongene, RIN1. Moreover, RIN1 knockdown completely blocked miR-3619-5p-enhanced RB progression. In summary, high LINC00202 levels are correlated with poor prognosis in RB, and it promotes RB progression by sponging miR-3619-5p and therefore up-regulating RIN1 expression.

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Section: Biotin Rna Pull-down Assaymentioning

confidence: 99%

Long Noncoding RNA LINC00202 Promotes Tumor Progression by Sponging miR-3619-5p in Retinoblastoma

Yan

et al. 2019

Cell Struct. Funct.

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“…Many non-coding RNAs have been reported to be involved in the regulation of cancer metabolism (18). For example, lncRNA PVT1 promotes glycolysis and tumor progression by regulating the miR-497/HK2 axis in osteosarcoma (19), whereas lncRNA-MIF inhibits aerobic glycolysis and tumorigenesis by suppressing c-Myc and miR-586 in cancer cells (20).…”

Section: Introductionmentioning

confidence: 99%

Long Non-coding RNA MEG3 Activated by Vitamin D Suppresses Glycolysis in Colorectal Cancer via Promoting c-Myc Degradation

Zuo

Wang

et al. 2020

Front. Oncol.

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Colorectal cancer (CRC), a common tumor, is characterized by a high mortality rate. Long non-coding RNA maternally expressed gene 3 (MEG3) serves a regulatory role in the carcinogenesis and progression of several types of cancer; however, its role in CRC remains largely unknown. The aim of this study was to explore the regulatory role and mechanism(s) of MEG3 in CRC. The Warburg effect or aerobic glycolysis is characteristic of the metabolism of tumor cells. To determine the effect of MEG3 on glycolysis of CRC cells, we used an XF analyzer to perform glycolysis stress test assays and found that overexpression of MEG3 significantly inhibited glycolysis, glycolytic capacity, as well as lactate production in CRC cells, whereas knockdown of MEG3 produced the opposite effect. Mechanistically, overexpression of MEG3 induced ubiquitin-dependent degradation of c-Myc and inhibited c-Myc target genes involved in the glycolysis pathway such as lactate dehydrogenase A, pyruvate kinase muscle 2, and hexokinase 2. Moreover, we found that MEG3 can be activated by vitamin D and vitamin D receptor (VDR). Clinical data demonstrated that MEG3 was positively associated with serum vitamin D concentrations in patients with CRC. We found that 1,25(OH) 2 D 3 treatment increased MEG3 expression, and knockdown of VDR abolished the effect of MEG3 on glycolysis. These results indicate that vitamin D-activated MEG3 suppresses aerobic glycolysis in CRC cells via degradation of c-Myc. Thus, vitamin D may have therapeutic value in the treatment of CRC.

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“…c‐Myc is one of the most frequently amplified oncogenes, and its alteration is observed in >70% of all human cancers, including HCC . c‐Myc, as a master transcriptional factor, regulates approximately 10%‐15% of genes in the genome and thus plays critical roles in essential biological processes such as cell growth, proliferation, apoptosis, and differentiation . The significance of c‐Myc has been defined in HCC.…”

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confidence: 99%

Tumor Necrosis Factor Receptor–Associated Factor 6 Promotes Hepatocarcinogenesis by Interacting With Histone Deacetylase 3 to Enhance c‐Myc Gene Expression and Protein Stability

Yang

et al. 2019

Hepatology

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The oncogene c‐Myc is aberrantly expressed and plays a key role in malignant transformation and progression of hepatocellular carcinoma (HCC). Here, we report that c‐Myc is significantly up‐regulated by tumor necrosis factor receptor–associated factor 6 (TRAF6), an E3 ubiquitin ligase, in hepatocarcinogenesis. High TRAF6 expression in clinical HCC samples correlates with poor prognosis, and the loss of one copy of the Traf6 gene in Traf6+/– mice significantly impairs liver tumorigenesis. Mechanistically, TRAF6 first interacts with and ubiquitinates histone deacetylase 3 (HDAC3) with K63‐linked ubiquitin chains, which leads to the dissociation of HDAC3 from the c‐Myc promoter and subsequent acetylation of histone H3 at K9, thereby epigenetically enhancing the mRNA expression of c‐Myc. Second, the K63‐linked ubiquitination of HDAC3 impairs the HDAC3 interaction with c‐Myc and promotes c‐Myc protein acetylation, which thereby enhances c‐Myc protein stability by inhibiting carboxyl terminus of heat shock cognate 70‐kDa–interacting protein–mediated c‐Myc ubiquitination and degradation. Importantly, TRAF6/HDAC3/c‐Myc signaling is also primed in hepatitis B virus–transgenic mice, unveiling a critical role for a mechanism in inflammation–cancer transition. In clinical specimens, TRAF6 positively correlates with c‐Myc at both the mRNA and protein levels, and high TRAF6 and c‐Myc expression is associated with an unfavorable prognosis, suggesting that TRAF6 collaborates with c‐Myc to promote human hepatocarcinogenesis. Consistently, curbing c‐Myc expression by inhibition of TRAF6 activity with a TRAF6 inhibitor peptide or the silencing of c‐Myc by small interfering RNA significantly suppressed tumor growth in mice. Conclusion: These findings demonstrate the oncogenic potential of TRAF6 during hepatocarcinogenesis by modulating TRAF6/HDAC3/c‐Myc signaling, with potential implications for HCC therapy.

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LncRNA‐MIF, a c‐Myc‐activated long non‐coding RNA, suppresses glycolysis by promoting Fbxw7‐mediated c‐Myc degradation

Cited by 96 publications

References 52 publications

Long Noncoding RNA LINC00202 Promotes Tumor Progression by Sponging miR-3619-5p in Retinoblastoma

Long Noncoding RNA LINC00202 Promotes Tumor Progression by Sponging miR-3619-5p in Retinoblastoma

Long Non-coding RNA MEG3 Activated by Vitamin D Suppresses Glycolysis in Colorectal Cancer via Promoting c-Myc Degradation

Tumor Necrosis Factor Receptor–Associated Factor 6 Promotes Hepatocarcinogenesis by Interacting With Histone Deacetylase 3 to Enhance c‐Myc Gene Expression and Protein Stability

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