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Status |
Public on Sep 08, 2017 |
Title |
DNA microarray analysis of human colorectal cancer specimens |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by array
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Summary |
Cancer cells alter their metabolism for the production of precursors of macromolecules. However, the control mechanisms underlying this reprogramming are poorly understood. Here, we show that metabolic reprogramming of colorectal cancer is caused chiefly by aberrant MYC expression. Multi-omics-based analyses of paired normal and tumor tissues from 275 patients with colorectal cancer revealed that metabolic alterations occur at the adenoma stage of carcinogenesis, in a manner not associated with specific gene mutations involved in colorectal carcinogenesis. MYC expression induced at least 215 metabolic reactions by changing the expression levels of 121 metabolic genes and 39 transporter genes. Further, MYC negatively regulated the expression of genes involved in mitochondrial biogenesis and maintenance but positively regulated genes involved in DNA and histone methylation. Knockdown of MYC in colorectal cancer cells reset the altered metabolism and suppressed cell growth. Moreover, inhibition of MYC target pyrimidine synthesis genes such as CAD, UMPS and CTPS blocked cell growth, and thus they are potential targets for colorectal cancer therapy.
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Overall design |
Gene expression in paired normal and tumor tissue specimens from patients with colorectal cancer.
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Contributor(s) |
Satoh K, Yachida S, Sugimoto M, Oshima M, Nakagawa T, Akamoto S, Okano K, Suzuki Y, Soga T |
Citation(s) |
28847964 |
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Submission date |
Oct 24, 2016 |
Last update date |
Mar 27, 2018 |
Contact name |
Kiyotoshi Satoh |
Organization name |
Keio University
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Department |
Institute for Advanced Biosciences
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Street address |
Mizukami 246-2, Kakuganji
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City |
Tsuruoka |
State/province |
Yamagata |
ZIP/Postal code |
997-0052 |
Country |
Japan |
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Platforms (1) |
GPL16699 |
Agilent-039494 SurePrint G3 Human GE v2 8x60K Microarray 039381 (Feature Number version) |
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Samples (80)
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Relations |
BioProject |
PRJNA350249 |