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Molecular Research of Glycolysis
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Molecular Research of Glycolysis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Macromolecules".

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 30434

Special Issue Editors

Prof. Dr. Cheorl-Ho Kim

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Guest Editor
1. Department of Biological Sciences, College of Science, Sungkyunkwan University, Seoburo 2066, Suwon 16419, Republic of Korea
2. Samsung Advanced Institute of Health Science and Technology (SAIHST), Sungkyunkwan University, Seoul 06351, Republic of Korea
Interests: glycobiology; sialobiology; sialyltransferase; N-glycan; O-glycan; glycolipid; sphingolipid; glycoprotein; surface sugar; ganglioside; sialic acid; sialyl Le antigen; lectin; galectin; siglec; ER-Golgi glyosylation; sugar–receptor interaction; innate immune; xenotransplantation; cell–cell interaction
Special Issues, Collections and Topics in MDPI journals
Dr. Yu-Chan Chang

E-Mail Website
Guest Editor
Department of Biomedicine Imaging and Radiological Science, National Yang Ming Chiao Tung University, Taipei 112, Taiwan
Interests: cancer metabolism; radiobiology; biomolecular imaging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Monosaccharide (glucose) is considered being the basic unit and main nutrient resource for maintaining human physiological functions and metabolism. For glucose uptake in the human body, glycolysis will cause a cascade of catalysis and transformations. Metabolic reprogramming and related enzyme activity abnormalities are regarded as the key factors related to chronic diseases, inflammation, and even carcinogenesis. In addition to typical metabolic functions, glycolytic enzymes have also discovered their genetic alterations, signal transduction, protein interactions and prognostic value.

We encourage the publication of original research articles and comments that cover all aspects of glycolytic enzymes.

Contributions to this Special Issue will provide new insights into the mechanisms and functions of glycolytic genes, deepen our understanding of their biological role in health and disease, and reveal novel aspects of therapeutic opportunities.

Prof. Dr. Cheorl-Ho Kim
Prof. Dr. Yu-Chan Chang
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • glycolysis
  • metabolic reprogramming
  • regulation
  • signaling transduction
  • metabolites
  • biosensors

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Related Special Issue

Published Papers (7 papers)

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Editorial

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2 pages, 189 KiB  
Editorial
Molecular Research of Glycolysis
by Yu-Chan Chang and Cheorl-Ho Kim
Int. J. Mol. Sci. 2022, 23(9), 5052; https://doi.org/10.3390/ijms23095052 - 2 May 2022
Cited by 6 | Viewed by 2680
Abstract
Glycolysis represents the process of breaking down monosaccharides, which involves the energy metabolism, homeostasis, and the linkage of various physiological functions such as muscle movement, development, neurotransmission, etc [...] Full article
(This article belongs to the Special Issue Molecular Research of Glycolysis)

Research

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18 pages, 1170 KiB  
Article
Genetic and Physiological Characterization of Fructose-1,6-Bisphosphate Aldolase and Glyceraldehyde-3-Phosphate Dehydrogenase in the Crabtree-Negative Yeast Kluyveromyces lactis
by Rosaura Rodicio, Hans-Peter Schmitz and Jürgen J. Heinisch
Int. J. Mol. Sci. 2022, 23(2), 772; https://doi.org/10.3390/ijms23020772 - 11 Jan 2022
Cited by 7 | Viewed by 2835
Abstract
The milk yeast Kluyveromyces lactis degrades glucose through glycolysis and the pentose phosphate pathway and follows a mainly respiratory metabolism. Here, we investigated the role of two reactions which are required for the final steps of glucose degradation from both pathways, as well [...] Read more.
The milk yeast Kluyveromyces lactis degrades glucose through glycolysis and the pentose phosphate pathway and follows a mainly respiratory metabolism. Here, we investigated the role of two reactions which are required for the final steps of glucose degradation from both pathways, as well as for gluconeogenesis, namely fructose-1,6-bisphosphate aldolase (FBA) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH). In silico analyses identified one gene encoding the former (KlFBA1), and three genes encoding isoforms of the latter (KlTDH1, KlTDH2, KlGDP1). Phenotypic analyses were performed by deleting the genes from the haploid K. lactis genome. While Klfba1 deletions lacked detectable FBA activity, they still grew poorly on glucose. To investigate the in vivo importance of the GAPDH isoforms, different mutant combinations were analyzed for their growth behavior and enzymatic activity. KlTdh2 represented the major glycolytic GAPDH isoform, as its lack caused a slower growth on glucose. Cells lacking both KlTdh1 and KlTdh2 failed to grow on glucose but were still able to use ethanol as sole carbon sources, indicating that KlGdp1 is sufficient to promote gluconeogenesis. Life-cell fluorescence microscopy revealed that KlTdh2 accumulated in the nucleus upon exposure to oxidative stress, suggesting a moonlighting function of this isoform in the regulation of gene expression. Heterologous complementation of the Klfba1 deletion by the human ALDOA gene renders K. lactis a promising host for heterologous expression of human disease alleles and/or a screening system for specific drugs. Full article
(This article belongs to the Special Issue Molecular Research of Glycolysis)
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19 pages, 5599 KiB  
Article
Enhanced Platelet-Rich Plasma (ePRP) Stimulates Wound Healing through Effects on Metabolic Reprogramming in Fibroblasts
by Hsin-Pei Weng, Yuan-Yang Cheng, Hsin-Lun Lee, Tai-Yi Hsu, Yu-Tang Chang and Yao-An Shen
Int. J. Mol. Sci. 2021, 22(23), 12623; https://doi.org/10.3390/ijms222312623 - 23 Nov 2021
Cited by 14 | Viewed by 4388
Abstract
As a source of growth factors for expediting wound healing and tissue regeneration, plasma-rich plasma (PRP) has been extensively applied in diverse fields including orthopaedics, ophthalmology, oral and maxillofacial surgery, dentistry, and gynaecology. However, the function of PRP in metabolic regulations remains enigmatic. [...] Read more.
As a source of growth factors for expediting wound healing and tissue regeneration, plasma-rich plasma (PRP) has been extensively applied in diverse fields including orthopaedics, ophthalmology, oral and maxillofacial surgery, dentistry, and gynaecology. However, the function of PRP in metabolic regulations remains enigmatic. A standardized method was devised herein to enrich growth factors and to lyophilize it as enhanced PRP (ePRP) powder, which could become ubiquitously available without mechanical centrifugation in clinical practice. To identify metabolic reprogramming in human dermal fibroblasts under ePRP treatment, putative metabolic targets were identified by transcriptome profiling and validated for their metabolic effects and mechanism. ePRP does not only promote wound healing but re-aligns energy metabolism by shifting to glycolysis through stimulation of glycolytic enzyme activity in fibroblasts. On the contrary, oxygen consumption rates and several mitochondrial respiration activities were attenuated in ePRP-treated fibroblasts. Furthermore, ePRP treatment drives the mitochondrial resetting by hindering the mitochondrial biogenesis-related genes and results in a dampened mitochondrial mass. Antioxidant production was further increased by ePRP treatment to prevent reactive oxygen species formation. Besides, ePRP also halts the senescence progression of fibroblasts by activating SIRT1 expression. Importantly, the glycolytic inhibitor 2-DG can completely reverse the ePRP-enhanced wound healing capacity, whereas the mitochondrial inhibitor oligomycin cannot. This is the first study to utilize PRP for comprehensively investigating its effects on the metabolic reprogramming of fibroblasts. These findings indicate that PRP’s primary metabolic regulation is to promote metabolic reprogramming toward glycolytic energy metabolism in fibroblasts, preserving redox equilibrium and allowing anabolic pathways necessary for the healing and anti-ageing process. Full article
(This article belongs to the Special Issue Molecular Research of Glycolysis)
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22 pages, 15012 KiB  
Article
PDK1 Inhibitor BX795 Improves Cisplatin and Radio-Efficacy in Oral Squamous Cell Carcinoma by Downregulating the PDK1/CD47/Akt-Mediated Glycolysis Signaling Pathway
by Shin Pai, Vijesh Kumar Yadav, Kuang-Tai Kuo, Narpati Wesa Pikatan, Chun-Shu Lin, Ming-Hsien Chien, Wei-Hwa Lee, Michael Hsiao, Shao-Chih Chiu, Chi-Tai Yeh and Jo-Ting Tsai
Int. J. Mol. Sci. 2021, 22(21), 11492; https://doi.org/10.3390/ijms222111492 - 25 Oct 2021
Cited by 33 | Viewed by 3989
Abstract
Background: Oral squamous cell carcinoma (OSCC) has a high prevalence and predicted global mortality rate of 67.1%, necessitating better therapeutic strategies. Moreover, the recurrence and resistance of OSCC after chemo/radioresistance remains a major bottleneck for its effective treatment. Molecular targeting is one [...] Read more.
Background: Oral squamous cell carcinoma (OSCC) has a high prevalence and predicted global mortality rate of 67.1%, necessitating better therapeutic strategies. Moreover, the recurrence and resistance of OSCC after chemo/radioresistance remains a major bottleneck for its effective treatment. Molecular targeting is one of the new therapeutic approaches to target cancer. Among a plethora of targetable signaling molecules, PDK1 is currently rising as a potential target for cancer therapy. Its aberrant expression in many malignancies is observed associated with glycolytic re-programming and chemo/radioresistance. Methods: Furthermore, to better understand the role of PDK1 in OSCC, we analyzed tissue samples from 62 patients with OSCC for PDK1 expression. Combining in silico and in vitro analysis approaches, we determined the important association between PDK1/CD47/LDHA expression in OSCC. Next, we analyzed the effect of PDK1 expression and its connection with OSCC orosphere generation and maintenance, as well as the effect of the combination of the PDK1 inhibitor BX795, cisplatin and radiotherapy in targeting it. Results: Immunohistochemical analysis revealed that higher PDK1 expression is associated with a poor prognosis in OSCC. The immunoprecipitation assay indicated PDK1/CD47 binding. PDK1 ligation significantly impaired OSCC orosphere formation and downregulated Sox2, Oct4, and CD133 expression. The combination of BX795 and cisplatin markedly reduced in OSCC cell’s epithelial-mesenchymal transition, implying its synergistic effect. p-PDK1, CD47, Akt, PFKP, PDK3 and LDHA protein expression were significantly reduced, with the strongest inhibition in the combination group. Chemo/radiotherapy together with abrogation of PDK1 inhibits the oncogenic (Akt/CD47) and glycolytic (LDHA/PFKP/PDK3) signaling and, enhanced or sensitizes OSCC to the anticancer drug effect through inducing apoptosis and DNA damage together with metabolic reprogramming. Conclusions: Therefore, the results from our current study may serve as a basis for developing new therapeutic strategies against chemo/radioresistant OSCC. Full article
(This article belongs to the Special Issue Molecular Research of Glycolysis)
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Review

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21 pages, 1344 KiB  
Review
The Metabolism Reprogramming of microRNA Let-7-Mediated Glycolysis Contributes to Autophagy and Tumor Progression
by Chien-Hsiu Li and Chiao-Chun Liao
Int. J. Mol. Sci. 2022, 23(1), 113; https://doi.org/10.3390/ijms23010113 - 22 Dec 2021
Cited by 14 | Viewed by 4163
Abstract
Cancer is usually a result of abnormal glucose uptake and imbalanced nutrient metabolization. The dysregulation of glucose metabolism, which controls the processes of glycolysis, gives rise to various physiological defects. Autophagy is one of the metabolic-related cellular functions and involves not only energy [...] Read more.
Cancer is usually a result of abnormal glucose uptake and imbalanced nutrient metabolization. The dysregulation of glucose metabolism, which controls the processes of glycolysis, gives rise to various physiological defects. Autophagy is one of the metabolic-related cellular functions and involves not only energy regeneration but also tumorigenesis. The dysregulation of autophagy impacts on the imbalance of metabolic homeostasis and leads to a variety of disorders. In particular, the microRNA (miRNA) Let-7 has been identified as related to glycolysis procedures such as tissue repair, stem cell-derived cardiomyocytes, and tumoral metastasis. In many cancers, the expression of glycolysis-related enzymes is correlated with Let-7, in which multiple enzymes are related to the regulation of the autophagy process. However, much recent research has not comprehensively investigated how Let-7 participates in glycolytic reprogramming or its links to autophagic regulations, mainly in tumor progression. Through an integrated literature review and omics-related profiling correlation, this review provides the possible linkage of the Let-7 network between glycolysis and autophagy, and its role in tumor progression. Full article
(This article belongs to the Special Issue Molecular Research of Glycolysis)
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16 pages, 783 KiB  
Review
Glycolysis under Circadian Control
by Jana Zlacká and Michal Zeman
Int. J. Mol. Sci. 2021, 22(24), 13666; https://doi.org/10.3390/ijms222413666 - 20 Dec 2021
Cited by 15 | Viewed by 7207
Abstract
Glycolysis is considered a main metabolic pathway in highly proliferative cells, including endothelial, epithelial, immune, and cancer cells. Although oxidative phosphorylation (OXPHOS) is more efficient in ATP production per mole of glucose, proliferative cells rely predominantly on aerobic glycolysis, which generates ATP faster [...] Read more.
Glycolysis is considered a main metabolic pathway in highly proliferative cells, including endothelial, epithelial, immune, and cancer cells. Although oxidative phosphorylation (OXPHOS) is more efficient in ATP production per mole of glucose, proliferative cells rely predominantly on aerobic glycolysis, which generates ATP faster compared to OXPHOS and provides anabolic substrates to support cell proliferation and migration. Cellular metabolism, including glucose metabolism, is under strong circadian control. Circadian clocks control a wide array of metabolic processes, including glycolysis, which exhibits a distinct circadian pattern. In this review, we discuss circadian regulations during metabolic reprogramming and key steps of glycolysis in activated, highly proliferative cells. We suggest that the inhibition of metabolic reprogramming in the circadian manner can provide some advantages in the inhibition of oxidative glycolysis and a chronopharmacological approach is a promising way to treat diseases associated with up-regulated glycolysis. Full article
(This article belongs to the Special Issue Molecular Research of Glycolysis)
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22 pages, 1408 KiB  
Review
Current Development and Application of Anaerobic Glycolytic Enzymes in Urothelial Cancer
by Yi-Fang Yang, Hao-Wen Chuang, Wei-Ting Kuo, Bo-Syuan Lin and Yu-Chan Chang
Int. J. Mol. Sci. 2021, 22(19), 10612; https://doi.org/10.3390/ijms221910612 - 30 Sep 2021
Cited by 10 | Viewed by 2797
Abstract
Urothelial cancer is a malignant tumor with metastatic ability and high mortality. Malignant tumors of the urinary system include upper tract urothelial cancer and bladder cancer. In addition to typical genetic alterations and epigenetic modifications, metabolism-related events also occur in urothelial cancer. This [...] Read more.
Urothelial cancer is a malignant tumor with metastatic ability and high mortality. Malignant tumors of the urinary system include upper tract urothelial cancer and bladder cancer. In addition to typical genetic alterations and epigenetic modifications, metabolism-related events also occur in urothelial cancer. This metabolic reprogramming includes aberrant expression levels of genes, metabolites, and associated networks and pathways. In this review, we summarize the dysfunctions of glycolytic enzymes in urothelial cancer and discuss the relevant phenotype and signal transduction. Moreover, we describe potential prognostic factors and risks to the survival of clinical cancer patients. More importantly, based on several available databases, we explore relationships between glycolytic enzymes and genetic changes or drug responses in urothelial cancer cells. Current advances in glycolysis-based inhibitors and their combinations are also discussed. Combining all of the evidence, we indicate their potential value for further research in basic science and clinical applications. Full article
(This article belongs to the Special Issue Molecular Research of Glycolysis)
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