Abstract
Antitumor drug therapy plays a very important role in cancer treatment. However, resistance to chemotherapy is a serious issue. Many studies have been conducted to understand and verify the cause of chemoresistance from multiple points of view such as oncogenes, tumor suppressor genes, DNA mutations and repairs, autophagy, cancer stemness, and mitochondrial metabolism and alteration. Nowadays, not only medical data from hospitals but also public big data exist on internet websites. Consequently, the importance of computational science has vastly increased in biological and medical sciences. Using statistical or mathematical analyses of these medical data with conventional experiments, many researchers have recently shown that there is a strong relationship between the biological metabolism and chemoresistance for cancer therapy. For example, folate metabolism that mediates one-carbon metabolism and polyamine metabolism have garnered attention regarding their association with cancer. It has been suggested that these metabolisms may be involved in causing resistance to chemotherapy.
Highlights
Incidence of cancer is increasing worldwide, and there are some challenges in cancer treatment, including resistance to antitumor drugs
Several studies have investigated the causes of chemotherapy resistance from multiple points of view such as oncogenes, tumor suppressor genes, DNA mutations and repairs, autophagy, cancer stemness, and mitochondrial metabolism and alteration[1,2,3,4,5,6,7]
It has been recently determined that differences in the biological metabolism pathways regarding the presence or absence of the characteristic of chemoresistance are related to drug resistance in cancer therapy
Summary
Incidence of cancer is increasing worldwide, and there are some challenges in cancer treatment, including resistance to antitumor drugs. It was reported that Raf/MEK/ERK pathway had an important role to drug resistance[43] This pathway is a signal transduction system responsible for cell growth, and the abnormal activation of this pathway is known that normal cells turn into cancer cells. It has been reported that EMT contributes to tumor progression by enhancing the infiltrative metastatic potential of cancer cells[71,72] and by increasing the resistance to antitumor drugs[73]. One of the trans-omics method developed by by Kosekiet al.[85] and Konno et al.[86] has been groundbreaking in identifying some biological metabolisms that may be involved in anticancer drug resistance in cancer cells. Application of computational analyses in this manner has made it possible to identify biological reactions that contribute to antitumor drug resistance
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