Saturday, July 10, 2021 11:22:40 PM
1. Introduction
Cancer is a group of diseases characterised by uncontrolled abnormal cell growth.
In 90–95%, cancer is caused by genetic mutations associated with environmental and
lifestyle factors, while 5–10% is connected with inherited genetics [1]. The activation of
oncogenes and the inactivation of tumour suppressor genes contributes to carcinogenesis.
Various mutations are reported in well-characterised cancer genes but the whole process of
carcinogenesis remains a mystery [2]. The genome instability leads to cancer development
by tumour angiogenesis, uncontrolled proliferation of cancer cells which are resistant
to death and avoid growth suppressors. Malignant cells can invade nearby tissue or
metastasize and avoid the immune system [3]. Furthermore, carcinogenesis leads to
changes in energy metabolism of cells [4]. Growing tumour cells produce a high level of
lactate during aerobic glycolysis. Tumour mitochondria are characterised by an increased
level of ROS, hypoxia and signals inhibiting apoptosis [5]. Most of the mtDNA somatic
mutations in tumours have been also reported as polymorphisms in the general population.
MtDNA mutations occur in various diseases. They are a disorder associated especially with
metabolism and energy [6]. In this review, we focus on the changes in mitochondrial DNA
associated with cancer (and other diseases), as well as on the function of mitochondria in
human cells.
https://www.mdpi.com/1422-0067/22/10/5100/pdf
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