miR‐290/371‐Mbd2‐Myc circuit regulates glycolytic metabolism to promote pluripotency

Cao, Yang; Guo, Wen; Tian, Shengya; He, Xiaoping; Wang, Xi Wen; Liu, Xiaomeng; Gu, Kai Li; Ma, Xiaoyu; Huang, De; Hu, Lan; Cai, Yongping; Zhang, Huafeng; Wang, Yangming

doi:10.15252/embj.201490441

Cited by 80 publications

(87 citation statements)

References 66 publications

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“…There was no significant difference for PKM2 mRNA in the breast cancer with miR-122-5p or the miRNA control transfection, but, PKM2 protein showed down-regulation in the cells. HK2 was regulated by miR-143 [24], miR-155 [25], miR-199a-5p [26], miR-29b [27,[28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43], miR-140-5p in various cancers like bladder cancer, liver cancer and prostate cancer. LDHA was regulated by miR-383, miR34a, miR-122, miR-30a-5p and other miRNAs in cancer.…”

Section: Discussionmentioning

confidence: 99%

WITHDRAWN: Lack of miR-216b-5p, miR-33a-5p or miR-122-5p in MSCs exosomes promotes breast cancer glycolysis by targeting HK2, LDHA and PKM2

Xia¹,

Yu²,

Mao³

et al. 2018

Oncotarget

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Exosomes contain many important components including miRNAs for cancerstromal communication. Mesenchymal stromal cells support tumor development, however, the low expression of miRNAs in exosomes and their regulation roles from mesenchymal stromal cells are still unclear. In this study, we hypothesized that mesenchymal stromal cells-derived exosomes promote breast cancer cell glycolysis. Our results showed that mesenchymal stromal cells-derived exosomes promoted cell proliferation and glycolysis of breast cancer cells. Furthermore, sequencing of exosomal RNAs revealed miR-216b-5p, miR-33a-5p and miR-122-5p were lack of expression in exosomes from mesenchymal stromal cells. MiR-216b-5p, miR-33a-5p and miR-122-5p overexpression in breast cancer cells suppressed glycolysis by targeting HK2, LDHA and PKM2 respectively. These results provided valuable insights and mechanism of mesenchymal stromal cells-secreted exosomes on the glycolysis of breast cancer.

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Section: Discussionmentioning

confidence: 99%

WITHDRAWN: Lack of miR-216b-5p, miR-33a-5p or miR-122-5p in MSCs exosomes promotes breast cancer glycolysis by targeting HK2, LDHA and PKM2

Xia¹,

Yu²,

Mao³

et al. 2018

Oncotarget

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show abstract

“…For example, p65, which is involved in modulating stem cell pluripotency, was identified as a new target for the miR-290 cluster (38). The miR-290 cluster has also been reported to stimulate glycolysis by regulating the glycolytic enzymes PKM2 and LDHA (39). To date, the study of the miR-290 -295 cluster has been limited to early embryos and stem cells.…”

Section: Discussionmentioning

confidence: 99%

Liver MicroRNA-291b-3p Promotes Hepatic Lipogenesis through Negative Regulation of Adenosine 5′-Monophosphate (AMP)-activated Protein Kinase α1

Meng

Guo

Fang

et al. 2016

Journal of Biological Chemistry

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In a microarray study, we found that hepatic miR-291b-3p was significantly increased in leptin-receptor-deficient type 2 mice (db/db), a mouse model of diabetes. The function of miR291b-3p is unknown. The potential role of miR-291b-3p in regulating hepatic lipid metabolism was explored in this study. High-fat diet (HFD)-and chow-fed mice were injected with an adenovirus expressing a miR-291b-3p inhibitor and a miR291b-3p mimic through the tail vein. Hepatic lipids and lipogenic gene expression were analyzed. Additionally, gain-and loss-of-function studies were performed in vitro to identify direct targets of miR-291b-3p. MiR-291b-3p expression and the protein levels of sterol regulatory element-binding protein 1 (SREBP1) and fatty acid synthase (FAS) were increased in the steatotic liver of db/db mice and HFD-fed mice versus their respective controls. Inhibition of hepatic miR-291b-3p expression prevented increases in hepatic lipogenesis and steatosis in HFD-fed mice. The opposite was observed when miR-291b-3p was overexpressed in the livers of chow-fed C57BL/6J wild-type mice. In vitro studies revealed that silencing of miR-291b-3p in NCTC1469 hepatic cells ameliorated oleic acid/palmitic acid mixture-induced elevation of cellular triglycerides. Importantly, we identified AMP-activated protein kinase (AMPK)-␣1 as a direct target of miR-291b-3p. Using metformin, an activator of AMPK, we showed that AMPK activation-induced inhibition of hepatic lipid accumulation was accompanied by reduced expression of miR-291b-3p in the liver. Liver miR-291b-3p promoted hepatic lipogenesis and lipid accumulation in mice. AMPK␣1 is a direct target of miR-291b-3p. In conclusion, our findings indicate that miR-291b-3p promotes hepatic lipogenesis by suppressing AMPK␣1 expression and activity, indicating the therapeutic potential of miR-291b-3p inhibitors in fatty liver disease.

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“…Myc in turn upregulates the levels of the glycolytic enzymes Ldha and Pkm2 culminating in enhanced glycolysis. Analogously, the human miR-371 cluster, a homolog of the murine miR-290 cluster, exerts the same effect in hESCs (21).…”

Section: Micrornas and Pluripotent Stem Cellsmentioning

confidence: 94%

Function and significance of MicroRNAs in benign and malignant human stem cells

Utikal

Abba

Novak

et al. 2015

Seminars in Cancer Biology

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miR‐290/371‐Mbd2‐Myc circuit regulates glycolytic metabolism to promote pluripotency

Cited by 80 publications

References 66 publications

WITHDRAWN: Lack of miR-216b-5p, miR-33a-5p or miR-122-5p in MSCs exosomes promotes breast cancer glycolysis by targeting HK2, LDHA and PKM2

WITHDRAWN: Lack of miR-216b-5p, miR-33a-5p or miR-122-5p in MSCs exosomes promotes breast cancer glycolysis by targeting HK2, LDHA and PKM2

Liver MicroRNA-291b-3p Promotes Hepatic Lipogenesis through Negative Regulation of Adenosine 5′-Monophosphate (AMP)-activated Protein Kinase α1

Function and significance of MicroRNAs in benign and malignant human stem cells

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