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Biomolecules
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Role of the Mitochondrial Stress Response in Human Cancer Progression
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Role of the Mitochondrial Stress Response in Human Cancer Progression

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Chemical Biology".

Deadline for manuscript submissions: closed (15 November 2021) | Viewed by 5556

Special Issue Editor

Prof. Dr. Hsin-Chen Lee

E-Mail Website
Guest Editor
Institute of Pharmacology, National Yang Ming Chiao Tung University, Taipei, Taiwan
Interests: mitochondrial dysfunction; mitochondrial DNA mutation; retrograde signaling; integrated stress response; oxidative stress; cell death; cancer progression

Special Issue Information

Dear Colleagues,

Deregulation of cellular energetics has been identified as one of the hallmarks of cancer. Increasing evidence shows that somatic mutation in mitochondrial DNA (mtDNA), alteration in mtDNA copy number, mitochondrial enzyme defect, and mitochondrial dynamic change may contribute to mitochondrial dysfunction in cancer cells. Communication from mitochondria to the nucleus that is retrograde signaling is suggested to be involved in the mechanism that underlies mitochondrial dysfunction, ultimately promoting cancer malignant progression. Recent studies have suggested that several signaling pathways or mitochondrion-derived molecules might act as retrograde signaling regulators in the development and progression of cancer. However, the detailed molecular mechanisms by which alterations in mitochondrial function and metabolism promote cancer progression are cancer-type dependent and are yet to be studied.

In this Special Issue, we aim to promote the progression and development of the field relating to the role of mitochondria in cancer progression, as well as to the development of the strategies targeting the components of mitochondrial signaling for cancer treatment. We look for innovative research that is capable of dissecting the role of mitochondrial alteration or retrograde signaling in cancer progression. Original manuscripts and reviews dealing with any aspect of the role of alterations in mitochondrial function and metabolism involved in cancer malignant progression are welcomed.

Prof. Dr. Hsin-Chen Lee
Guest Editor

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. Biomolecules is an international peer-reviewed open access monthly 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

  • mitochondrial dysfunction
  • MtDNA mutation
  • retrograde signaling
  • integrated stress response
  • oxidative stress
  • cancer progression

Published Papers (2 papers)

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Research

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16 pages, 1341 KiB  
Article
Levels of Coenzyme Q10 and Several COQ Proteins in Human Astrocytoma Tissues Are Inversely Correlated with Malignancy
by Hsiu-Chuan Yen, Bing-Shian Chen, Si-Ling Yang, Shin-Yu Wu, Chun-Wei Chang, Kuo-Chen Wei, Jee-Ching Hsu, Yung-Hsing Hsu, Tzung-Hai Yen and Chih-Lung Lin
Biomolecules 2022, 12(2), 336; https://0-doi-org.brum.beds.ac.uk/10.3390/biom12020336 - 20 Feb 2022
Cited by 3 | Viewed by 1946
Abstract
In a previous study, we reported the alterations of primary antioxidant enzymes and decreased citrate synthase (CS) activities in different grades of human astrocytoma tissues. Here, we further investigated coenzyme Q10 (CoQ10) levels and protein levels of polyprenyl diphosphate synthase [...] Read more.
In a previous study, we reported the alterations of primary antioxidant enzymes and decreased citrate synthase (CS) activities in different grades of human astrocytoma tissues. Here, we further investigated coenzyme Q10 (CoQ10) levels and protein levels of polyprenyl diphosphate synthase subunit (PDSS2) and several COQ proteins required for CoQ10 biosynthesis in these tissues. We found that the level of endogenous CoQ10, but not of exogenous α-tocopherol, was higher in nontumor controls than in all grades of astrocytoma tissues. The levels of COQ3, COQ5, COQ6, COQ7, COQ8A, and COQ9, but not of COQ4, were lower in Grade IV astrocytoma tissues than in controls or low-grade (Grades I and II) astrocytomas, but PDSS2 levels were higher in astrocytoma tissues than in controls. Correlation analysis revealed that the levels of CoQ10 and COQ proteins were negatively correlated with malignancy degree and positively correlated with CS activity, whereas PDSS2 level was positively correlated with malignancy. Moreover, lower level of mitochondrial DNA-encoded cytochrome c oxidase subunit 2 was not only associated with a higher malignancy degree but also with lower level of all COQ proteins detected. The results revealed that mitochondrial abnormalities are associated with impaired CoQ10 maintenance in human astrocytoma progression. Full article
(This article belongs to the Special Issue Role of the Mitochondrial Stress Response in Human Cancer Progression)
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Review

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11 pages, 1607 KiB  
Review
An Asp to Strike Out Cancer? Therapeutic Possibilities Arising from Aspartate’s Emerging Roles in Cell Proliferation and Survival
by Iiro Taneli Helenius, Hanumantha Rao Madala and Jing-Ruey Joanna Yeh
Biomolecules 2021, 11(11), 1666; https://0-doi-org.brum.beds.ac.uk/10.3390/biom11111666 - 10 Nov 2021
Cited by 10 | Viewed by 2847
Abstract
A better understanding of the metabolic constraints of a tumor may lead to more effective anticancer treatments. Evidence has emerged in recent years shedding light on a crucial aspartate dependency of many tumor types. As a precursor for nucleotide synthesis, aspartate is indispensable [...] Read more.
A better understanding of the metabolic constraints of a tumor may lead to more effective anticancer treatments. Evidence has emerged in recent years shedding light on a crucial aspartate dependency of many tumor types. As a precursor for nucleotide synthesis, aspartate is indispensable for cell proliferation. Moreover, the malate–aspartate shuttle plays a key role in redox balance, and a deficit in aspartate can lead to oxidative stress. It is now recognized that aspartate biosynthesis is largely governed by mitochondrial metabolism, including respiration and glutaminolysis in cancer cells. Therefore, under conditions that suppress mitochondrial metabolism, including mutations, hypoxia, or chemical inhibitors, aspartate can become a limiting factor for tumor growth and cancer cell survival. Notably, aspartate availability has been associated with sensitivity or resistance to various therapeutics that are presently in the clinic or in clinical trials, arguing for a critical need for more effective aspartate-targeting approaches. In this review, we present current knowledge of the metabolic roles of aspartate in cancer cells and describe how cancer cells maintain aspartate levels under different metabolic states. We also highlight several promising aspartate level-modulating agents that are currently under investigation. Full article
(This article belongs to the Special Issue Role of the Mitochondrial Stress Response in Human Cancer Progression)
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