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J Cell Physiol. 2019 May;234(5):5601-5612. doi: 10.1002/jcp.27388. Epub 2018 Oct 20.

Strategies to target energy metabolism in consensus molecular subtype 3 along with Kirsten rat sarcoma viral oncogene homolog mutations for colorectal cancer therapy.

Author information

1
Department of Pharmaceutics, Shanghai Eighth People's Hospital, Jiangsu University, Shanghai, China.
2
Interventional Cancer Institute of Chinese Integrative Medicine, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
3
Department of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.

Abstract

Alterations in cellular energy metabolism play a critical role in colorectal cancer (CRC), which has been identified as the definition of consensus molecular subtypes (CMSs), and CMS3 tumors exhibit energy metabolism signatures along with Kirsten rat sarcoma viral oncogene homolog (KRAS)-activating mutations. This review summarizes the relationship between CMS3 tumors associated with mutated KRAS and energy metabolism in CRC, especially for the dysregulated energy metabolism that affects tumor cell proliferation, invasion, and migration. Furthermore, this review concentrates on the role of metabolic genes and factors and signaling pathways, which coupled with a primary energy source connected with the CMS3 associated with mutated KRAS, induce metabolic alterations. The strategies to target energy metabolism for the metabolic alterations in mutated KRAS CRC are also introduced. In conclusion, dysregulated energy metabolism has a close relationship with mutated KRAS in CMS3 tumors. Therefore, selective inhibitors or agents against metabolic targets or KRAS signaling may be clinically useful for CMS3 tumor treatment through a personalized approach for patients with cancer.

KEYWORDS:

Kirsten rat sarcoma viral oncogene homolog (KRAS); colorectal cancers (CRCs); consensus molecular subtype 3 (CMS3); energy metabolism; therapy

PMID:
30341899
DOI:
10.1002/jcp.27388

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