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고려대학교

Exp. Mol. Med., Published 06 July 2022 | https://doi.org/10.1038/s12276-022-00795-z Augmentation of the RNA m6A reader signature is associated with poor survival by enhancing cell proliferation and EMT across cancer types

Jaeik Oh^1,2,9, Chanwoong Hwa^3,4,5,9, Dongjun Jang⁶, Seungjae Shin⁶, Soo-Jin Lee⁶, Jiwon Kim⁶, Sang Eun Lee⁶, Hae Rim Jung⁷, Yumi Oh⁷, Giyong Jang⁷, Obin Kwon^6,7, Joon-Yong An^3,4,* and Sung-Yup Cho^1,6,7,8,*

¹Department of Translational Medicine, Seoul National University College of Medicine, Seoul 03080, Korea. ²Department of Internal Medicine, Seoul National University Hospital, Seoul 03080, Korea. ³School of Biosystem and Biomedical Science, College of Health Science, Korea University, Seoul 02841, Korea. ⁴BK21FOUR R&E Center for Learning Health Systems, Korea University, Seoul 02841, Korea. ⁵Department of Integrated Biomedical and Life Science, Korea University, Seoul 02841, Korea. ⁶Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Korea. ⁷Medical Research Center, Genomic Medicine Institute, Seoul National University College of Medicine, Seoul 03080, Korea. ⁸Cancer Research Institute, Seoul National University, Seoul 03080, Korea. ⁹These authors contributed equally: Jaeik Oh, Chanwoong Hwa.

^*Corresponding author.

Abstract

N⁶-Methyladenosine (m6A) RNA modification plays a critical role in the posttranscriptional regulation of gene expression. Alterations in cellular m6A levels and m6A-related genes have been reported in many cancers, but whether they play oncogenic or tumor-suppressive roles is inconsistent across cancer types. We investigated common features of alterations in m6A modification and m6A-related genes during carcinogenesis by analyzing transcriptome data of 11 solid tumors from The Cancer Genome Atlas database and our in-house gastric cancer cohort. We calculated m6A writer (W), eraser (E), and reader (R) signatures based on corresponding gene expression. Alterations in the W and E signatures varied according to the cancer type, with a strong positive correlation between the W and E signatures in all types. When the patients were divided according to m6A levels estimated by the ratio of the W and E signatures, the prognostic effect of m6A was inconsistent according to the cancer type. The R and especially the R2 signatures (based on the expression of IGF2BPs) were upregulated in all cancers. Patients with a high R2 signature exhibited poor prognosis across types, which was attributed to enrichment of cell cycle- and epithelial–mesenchymal transition-related pathways. Our study demonstrates common features of m6A alterations across cancer types and suggests that targeting m6A R proteins is a promising strategy for cancer treatment.

논문정보

형식Research article
게재일2022년 07월 (BRIC 등록일 2022-08-12)
연구진국내 연구진
분야 의약학 > 종양의학

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