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Cells
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Signaling Pathways/Metabolic Reprogramming Crosstalk in Cancer Cells
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Signaling Pathways/Metabolic Reprogramming Crosstalk in Cancer Cells

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: closed (15 May 2023) | Viewed by 8027

Special Issue Editors

Dr. Pranabananda Dutta

E-Mail Website
Guest Editor
Department of Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA 90059, USA
Interests: cancer genomics; transcriptomics; cancer cell signaling; metabolism; DNA damage response
Dr. Kamrul Hasan

E-Mail Website
Guest Editor
Department of Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA 90059, USA
Interests: lipid metabolism; non-alcoholic fatty liver disease; transcription; cancer

Special Issue Information

Dear Colleagues,

We are excited to announce the launch of a new Special Issue on signaling and metabolic reprogramming cancer. Metabolic reprogramming in cancer involves switching from glycolysis and oxidative phosphorylation to aerobic glycolysis, a phenomenon known as the Warburg effect. This phenomenon is particularly true in solid cancer and is associated with tumor growth. The metabolic changes also reflect redox programming, nucleotide biosynthesis, and amino acid metabolism. In addition, multiple cellular signaling pathways regulate metabolism by regulating multiple factors in cellular homeostasis.

The Special Issue will examine potential modulators of cell metabolism, including glucose and glutamate metabolism, and dissect the relationship between cell signaling pathways. It will also focus on cancer cell lipid metabolism. In addition, it will focus on the role of the tumor microenvironment, particularly on immune cells, cancer-associated fibroblasts, and endothelial cells. Along with that, in vivo preclinical models to investigate the pathways or novel methodological approaches to determine metabolic burden in cancer patients with prognostic values will be crucial to this issue. Finally, health disparity related to cancer patients based on ancestry and novel therapy targeting cancer cell metabolism by focusing on enzymes and transporters will also be highlighted.

Dr. Pranabananda Dutta
Dr. Kamrul Hasan
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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • solid tumor
  • metabolic reprogramming
  • tumor microenvironment
  • immunotherapy and metabolism
  • targeting metabolic pathways
  • metabolic stress
  • lipid metabolism
  • Warburg effect
  • glutamine addiction

Published Papers (3 papers)

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Research

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22 pages, 3243 KiB  
Article
DCUN1D1 Is an Essential Regulator of Prostate Cancer Proliferation and Tumour Growth That Acts through Neddylation of Cullin 1, 3, 4A and 5 and Deregulation of Wnt/Catenin Pathway
by Akhona Vava, Juliano D. Paccez, Yihong Wang, Xuesong Gu, Manoj K. Bhasin, Michael Myers, Nelson C. Soares, Towia A. Libermann and Luiz F. Zerbini
Cells 2023, 12(15), 1973; https://doi.org/10.3390/cells12151973 - 31 Jul 2023
Cited by 2 | Viewed by 1770
Abstract
Defective in cullin neddylation 1 domain containing 1 (DCUN1D1) is an E3 ligase for the neddylation, a post-translational process similar to and occurring in parallel to ubiquitin proteasome pathway. Although established as an oncogene in a variety of squamous cell carcinomas, the precise [...] Read more.
Defective in cullin neddylation 1 domain containing 1 (DCUN1D1) is an E3 ligase for the neddylation, a post-translational process similar to and occurring in parallel to ubiquitin proteasome pathway. Although established as an oncogene in a variety of squamous cell carcinomas, the precise role of DCUN1D1 in prostate cancer (PCa) has not been previously explored thoroughly. Here, we investigated the role of DCUN1D1 in PCa and demonstrated that DCUN1D1 is upregulated in cell lines as well as human tissue samples. Inhibition of DCUN1D1 significantly reduced PCa cell proliferation and migration and remarkably inhibited xenograft formation in mice. Applying both genomics and proteomics approaches, we provide novel information about the DCUN1D1 mechanism of action. We identified CUL3, CUL4B, RBX1, CAND1 and RPS19 proteins as DCUN1D1 binding partners. Our analysis also revealed the dysregulation of genes associated with cellular growth and proliferation, developmental, cell death and cancer pathways and the WNT/β-catenin pathway as potential mechanisms. Inhibition of DCUN1D1 leads to the inactivation of β-catenin through its phosphorylation and degradation which inhibits the downstream action of β-catenin, reducing its interaction with Lef1 in the Lef1/TCF complex that regulates Wnt target gene expression. Together our data point to an essential role of the DCUN1D1 protein in PCa which can be explored for potential targeted therapy. Full article
(This article belongs to the Special Issue Signaling Pathways/Metabolic Reprogramming Crosstalk in Cancer Cells)
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Review

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23 pages, 908 KiB  
Review
Metabolic Pathways in Breast Cancer Reprograming: An Insight to Non-Coding RNAs
by Fereydoon Abedi-Gaballu, Elham Kamal Kazemi, Seyed Ahmad Salehzadeh, Behnaz Mansoori, Farhad Eslami, Ali Emami, Gholamreza Dehghan, Behzad Baradaran, Behzad Mansoori and William C. Cho
Cells 2022, 11(19), 2973; https://doi.org/10.3390/cells11192973 - 23 Sep 2022
Cited by 2 | Viewed by 3775
Abstract
Cancer cells reprogram their metabolisms to achieve high energetic requirements and produce precursors that facilitate uncontrolled cell proliferation. Metabolic reprograming involves not only the dysregulation in glucose-metabolizing regulatory enzymes, but also the enzymes engaging in the lipid and amino acid metabolisms. Nevertheless, the [...] Read more.
Cancer cells reprogram their metabolisms to achieve high energetic requirements and produce precursors that facilitate uncontrolled cell proliferation. Metabolic reprograming involves not only the dysregulation in glucose-metabolizing regulatory enzymes, but also the enzymes engaging in the lipid and amino acid metabolisms. Nevertheless, the underlying regulatory mechanisms of reprograming are not fully understood. Non-coding RNAs (ncRNAs) as functional RNA molecules cannot translate into proteins, but they do play a regulatory role in gene expression. Moreover, ncRNAs have been demonstrated to be implicated in the metabolic modulations in breast cancer (BC) by regulating the metabolic-related enzymes. Here, we will focus on the regulatory involvement of ncRNAs (microRNA, circular RNA and long ncRNA) in BC metabolism, including glucose, lipid and glutamine metabolism. Investigation of this aspect may not only alter the approaches of BC diagnosis and prognosis, but may also open a new avenue in using ncRNA-based therapeutics for BC treatment by targeting different metabolic pathways. Full article
(This article belongs to the Special Issue Signaling Pathways/Metabolic Reprogramming Crosstalk in Cancer Cells)
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Other

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13 pages, 961 KiB  
Perspective
LACTB, a Metabolic Therapeutic Target in Clinical Cancer Application
by Xiaohua Li, Zhongkai Ren, Xiaohong Huang and Tengbo Yu
Cells 2022, 11(17), 2749; https://doi.org/10.3390/cells11172749 - 3 Sep 2022
Cited by 1 | Viewed by 1902
Abstract
Serine beta-lactamase-like protein (LACTB) is the only mammalian mitochondrial homolog evolved from penicillin-binding proteins and β-lactamases (PBP-βLs) in bacteria. LACTB, an active-site serine protease, polymerizes into stable filaments, which are localized to the intermembrane space (IMS) of mitochondrion and involved in the submitochondrial [...] Read more.
Serine beta-lactamase-like protein (LACTB) is the only mammalian mitochondrial homolog evolved from penicillin-binding proteins and β-lactamases (PBP-βLs) in bacteria. LACTB, an active-site serine protease, polymerizes into stable filaments, which are localized to the intermembrane space (IMS) of mitochondrion and involved in the submitochondrial organization, modulating mitochondrial lipid metabolism. Cancer pathogenesis and progression are relevant to the alterations in mitochondrial metabolism. Metabolic reprogramming contributes to cancer cell behavior. This article (1) evidences the clinical implications of LACTB on neoplastic cell proliferation and migration and tumor growth and metastasis as well as LACTB’s involvement in chemotherapeutic and immunotherapeutic responses; (2) sketches the structural basis for LACTB activity and function; and (3) highlights the relevant regulatory mechanisms to LACTB. The abnormal expression of LACTB has been associated with clinicopathological features of cancer tissues and outcomes of anticancer therapies. With the current pioneer researches on the tumor-suppressed function, structural basis, and regulatory mechanism of LACTB, the perspective hints at a great appeal of enzymic property, polymerization, mutation, and epigenetic and post-translational modifications in investigating LACTB’s role in cancer pathogenesis. This perspective provides novel insights for LACTB as a metabolic regulator with potential to develop targeted cancer therapies or neoadjuvant therapeutic interventions. Full article
(This article belongs to the Special Issue Signaling Pathways/Metabolic Reprogramming Crosstalk in Cancer Cells)
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