Association between shortage of energy supply and nuclear gene mutations leading to carcinomatous transformation (Review)
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Affiliations: Department of Oncology, Anhui Provincial Hospital Affiliated to Anhui Medical University, Hefei, Anhui 230001, P.R. China
- Published online on: October 16, 2015 https://doi.org/10.3892/mco.2015.656
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11-12
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Abstract
Anaerobic bacteria use glycolysis, an oxygen‑independent metabolic pathway, whereas energy metabolism in the evolved eukaryotic cell is performed via oxidative phosphorylation, with all eukaryotic cell activities depending upon high energy consumption. However, in cancer cells evolving from eukaryotic cells, the energy metabolism switches from oxidative phosphorylation to glycolysis. The shortage of energy supply induces cancer cells to acquire specific characteristics. base pair renewal is the most energy‑consuming process in the cell, and shortage of energy supply may lead to errors in this process; the more prominent the shortage in energy supply, the more errors are likely to occur in base pair renewal, resulting in gene mutations and expression of cancer cell characteristics. Thus, shortage of energy supply is associated with carcinomatous transformation.
View References
1
|
Du J: Hypothesis of mitochondrial
oncogenesis as the trigger of normal cells to cancer cells. Med
Hypotheses. 82:744–747. 2014. View Article : Google Scholar : PubMed/NCBI
|
2
|
Sagan L: On the origin of mitosing cells.
J Theor Biol. 14:255–274. 1967. View Article : Google Scholar : PubMed/NCBI
|
3
|
Margulis L: Origin of eukaryotic cells.
New Haven: Yale University Press. Connecticut. 1970.
|
4
|
Grossgebauer K: Cancer: Re-evolution of
eukaryotic to prokaryotic replication units - a result of genetic
transposition? Biosystems. 16:253–258. 1984. View Article : Google Scholar
|
5
|
Grossgebauer K: Prokaryotic mechanisms in
eukaryotes: Experimental data and speculations. Med Hypotheses.
28:219–223. 1989. View Article : Google Scholar : PubMed/NCBI
|
6
|
Warburg O: The Metabolism of Tumors.
London: Arnold Constable. 1930.
|
7
|
Warburg O: On the origin of cancer cells.
Science. 123:309–314. 1956. View Article : Google Scholar : PubMed/NCBI
|
8
|
Enomoto K, Tanuma S and Yamada M: ATP
requirement for the processes of DNA replication in isolated HeLa
cell nuclei. J Biochem. 89:801–807. 1981.PubMed/NCBI
|
9
|
Scoccianti C, Vesin A, Martel G, Olivier
M, Brambilla E, Timsit JF, Tavecchio L, Brambilla C, Field JK and
Hainaut P: European Early Lung Cancer Consortium: Prognostic value
of TP53, KRAS and EGFR mutations in nonsmall cell lung cancer: The
EUELC cohort. Eur Respir J. 40:177–184. 2012. View Article : Google Scholar : PubMed/NCBI
|
10
|
Karsli-Ceppioglu S, Dagdemir A, Judes G,
Ngollo M, Penault-Llorca F, Pajon A, Bignon YJ and Bernard-Gallon
D: Epigenetic mechanisms of breast cancer: An update of the current
knowledge. Epigenomics. 6:651–664. 2014. View Article : Google Scholar : PubMed/NCBI
|
11
|
Mosalpuria K, Hall C, Krishnamurthy S,
Lodhi A, Hallman DM, Baraniuk MS, Bhattacharyya A and Lucci A:
Cyclooxygenase-2 expression in non-metastatic triple-negative
breast cancer patients. Mol Clin Oncol. 2:845–850. 2014.PubMed/NCBI
|
12
|
Wang W, Chen L, Tang Q, Fan Y, Zhang X and
Zhai J: Loss of ARHI expression in colon cancer and its clinical
significance. Contemp Oncol (Pozn). 18:329–333. 2014.PubMed/NCBI
|