Altered Mitochondrial Signalling and Metabolism in Cancer

Chattopadhyay, Esita; Roy, Bidyut

doi:10.3389/fonc.2017.00043

Cited by 32 publications

(21 citation statements)

References 182 publications

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“…In this study, PPARGC1A overexpression in rabbit one‐cell embryos increased the blastocyst percentage by regulating the mitochondrial biogenesis and metabolism during the embryo development, which indicates PPARGC1A expression level in the zygotes or oocytes might have important influences on early rabbit embryo development, supported by our previous research in goat oocytes (Zhang et al, ). In addition, we found high PPARGC1A level in the zygotes had a positive effect on the relative mtDNA copy numbers, the expressions of NRF1 and TFAM , energy production, and rabbit blastocyst percentage, in line with the previous results that PPARGC1A played positive effects on mitochondrial biogenesis (Chattopadhyay & Roy, ; Scarpulla, Vega, & Kelly, ), and NRF1 and TFAM promoted mitochondrial biogenesis in the embryo development (Larsson et al, ).…”

Section: Discussionsupporting

confidence: 90%

“…oocytes (Zhang et al, 2013). In addition, we found high PPARGC1A level in the zygotes had a positive effect on the relative mtDNA copy numbers, the expressions of NRF1 and TFAM, energy production, and rabbit blastocyst percentage, in line with the previous results that PPARGC1A played positive effects on mitochondrial biogenesis (Chattopadhyay & Roy, 2017;Scarpulla, Vega, & Kelly, 2012), and NRF1 and TFAM promoted mitochondrial biogenesis in the embryo development (Larsson et al, 1998).…”

Section: Expression Of Metabolite-related Genes In Ppargc1a Microinsupporting

confidence: 91%

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Effect of PPARGC1A on the development and metabolism of early rabbit embryos in vitro

Zhang

Guo

Deng

et al. 2019

Molecular Reproduction Devel

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Peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PPARGC1A) is a central regulator of mitochondrial biogenesis and metabolism, and its expression is closely related to embryo development. To gain insights into the possible mechanisms of PPARGC1A during early embryogenesis, the development potential, mitochondrial biogenesis, and the culture medium metabolomics of embryos were evaluated when PPARGC1A overexpressed or suppressed in rabbit zygotes. Results showed that different PPARGC1A levels in rabbit zygotes could affect blastocyst percentage, and the expressions of mitochondrial biogenesis and metabolic‐related genes, as well as the glutathione and adenosine triphosphate levels during early embryo development. In addition, compared with the controls, 12 and 10 different metabolites involved in carbohydrate, amino acid, and fatty acid metabolism were screened in the 5 day's spent culture medium of PPARGC1A overexpressed and suppressed embryos by gas chromatography–mass spectrometer, respectively. Consistent with these metabolite changes, the transcriptions of genes encoding glucose transporters and fatty acid biosynthetic proteins in the embryos from different groups were regulated by PPARGC1A during rabbit embryo development. Taken together, these data provide evidence that PPARGC1A may regulate early rabbit embryo development through mitochondrial biogenesis and metabolism.

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Section: Discussionsupporting

confidence: 90%

Section: Expression Of Metabolite-related Genes In Ppargc1a Microinsupporting

confidence: 91%

Effect of PPARGC1A on the development and metabolism of early rabbit embryos in vitro

Zhang

Guo

Deng

et al. 2019

Molecular Reproduction Devel

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“…Understanding the complexity of mitochondria functions became a challenging area of research over the past few years, with implications in the fields of regenerative medicine, oncology and immunology. This stems from the discovery that the mitochondria-dependent metabolic reprogramming controls a wealth of different functions: the self-renewal and differentiation capacities of mesenchymal (MSCs) and embryonic (ES) stem cells [3][4][5], the secretion of inflammatory cytokines by immune cells such as macrophages [6][7][8] and dendritic cells [8][9][10] and also the malignant properties of cancer cells [11,12].…”

Section: Introductionmentioning

confidence: 99%

Intercellular mitochondria trafficking highlighting the dual role of mesenchymal stem cells as both sensors and rescuers of tissue injury

et al. 2018

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Mitochondria are crucial organelles that not only regulate the energy metabolism, but also the survival and fate of eukaryotic cells. Mitochondria were recently discovered to be able to translocate from one cell to the other. This phenomenon was observed in vitro and in vivo, both in physiological and pathophysiological conditions including tissue injury and cancer. Mitochondria trafficking was found to exert prominent biological functions. In particular, several studies pointed out that this process governs some of the therapeutic effects of mesenchymal stem cells (MSCs). In this review, we give an overview of the current knowledge on MSC-dependent intercellular mitochondria trafficking and further discuss the recent findings on the intercellular mitochondria transfer between differentiated and mesenchymal stem cells, their biological significance and the mechanisms underlying this process.

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“…Pyruvate kinase M2 (PKM2), a key enzyme in glycolysis, is found to be frequently overexpressed in cancers and stimulates cell proliferation, migration, and invasion. 15,16 Previous research has shown that PKM2 is highly expressed in osteosarcoma and is associated with a poor outcome. 17 However, the association between miR-1294 and PKM2 in osteosarcoma has not been studied.…”

Section: Introductionmentioning

confidence: 99%

<p>Antitumor Effect of miR-1294/Pyruvate Kinase M2 Signaling Cascade in Osteosarcoma Cells</p>

Yuan¹,

Yu²,

Chen³

et al. 2020

OTT

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Background: MicroRNAs (miRNAs) can act as negative regulators of gene expression, and play a crucial role in cancer progression. The aim of this study was to investigate the role of miR-1294/pyruvate kinase M2 (PKM2) axis in osteosarcoma cells in vitro and in vivo. Methods: The function of miR-1294 and its association with PKM2 in osteosarcoma cells were studied by real-time PCR, CCK-8, Western blot, scratch test, transwell assay, flow cytometry, and dual-luciferase reporter assays. The effect of miR-1294 on tumor growth in vivo was evaluated in a subcutaneous xenograft model of osteosarcoma. Results: miR-1294 was downregulated in osteosarcoma cells. Forced overexpression of miR-1294 inhibited cell proliferation, migration, and invasion, and induced G0/G1 arrest and apoptosis. Consistently, protein expression levels of proliferating cell nuclear antigen, c-Myc, cyclin D1, active matrix metalloproteinase 2, and active matrix metalloproteinase 9 were decreased, and cleaved caspase 3 and cleaved PARP were increased following miR-1294 overexpression. Moreover, we demonstrated that PKM2 was a target of miR-1294 in osteosarcoma cells, and the effects caused by miR-1294 mimic were reversed by the overexpression of PKM2. Furthermore, we found that upregulation of miR-1294 inhibited tumorigenesis of osteosarcoma cells in vivo, which was accompanied by downregulation of PKM2. Conclusion: Our results revealed that miR-1294/PKM2 signaling cascade exerts important roles in the regulation of tumor progression, implying that this pathway may serve as a potential therapeutic target in osteosarcoma.

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Altered Mitochondrial Signalling and Metabolism in Cancer

Cited by 32 publications

References 182 publications

Effect of PPARGC1A on the development and metabolism of early rabbit embryos in vitro

Effect of PPARGC1A on the development and metabolism of early rabbit embryos in vitro

Intercellular mitochondria trafficking highlighting the dual role of mesenchymal stem cells as both sensors and rescuers of tissue injury

<p>Antitumor Effect of miR-1294/Pyruvate Kinase M2 Signaling Cascade in Osteosarcoma Cells</p>

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