Abstract
Colorectal cancer (CRC) represents one of the most common malignancies with high morbidity worldwide. RNA methylation (m6A) has been considered to tremendously contribute to cancer initiation and progression since its first discovery. In this study, we comprehensively analyzed associations between mRNA expressions of m6A regulators and CRC tumor samples' epidemiologic information from the Cancer Genome Atlas (TCGA). Multivariate Cox proportional hazard model was applied to screening of m6A regulators whose mRNA expressions were significantly associated with CRC tumor samples' overall survival (OS) probability and those significant regulators were used for LASSO regression analysis to construct CRC prognosis prediction signature. As a result, two regulators i.e., YTHDC2 and ALKBH5 were picked out in multivariate analysis. CRC prognosis signature was constructed based on those two regulators through which CRC tumor samples with favorable and inferior prognosis could definitely be distinguished independent of potential confounding factors. This study should be helpful for identifying prognostic different CRC patients and guiding therapeutic method selection.
Highlights
According to the global burden of disease study in 2018, colorectal cancer (CRC) is one of the most common cancer types worldwide, and represents the third leading cause of cancer-related deaths [1]
MRNA expressions of those regulators in CRC tumor and adjacent normal tissues from the Cancer Genome Atlas (TCGA) were obtained for constructing CRC prognosis prediction model
CRC tumor samples were further divided into different stages, i.e., stage I-IV, and the 12 regulators’ mRNA expressions were provided as boxplots (Figure 1B)
Summary
According to the global burden of disease study in 2018, colorectal cancer (CRC) is one of the most common cancer types worldwide, and represents the third leading cause of cancer-related deaths [1]. Many risk factors have been associated with CRC, including genetic and environmental factors. Increasingly researches have focused on the multiple molecular pathways involved in CRC pathogenesis, especially genetic and epigenetic events [3, 4]. It is generally believed that, epigenetic alterations in CRC occur earlier and happened more frequently than genetic alterations [5, 6]. Mutational inactivation of tumor suppressor genes, and activation of oncogenes are all involved in its development [6]. Genome-wide association studies have recently linked CRC to several common genetic variants or single-nucleotide polymorphisms, miRNA profiling of CRCs has identified over 20 up and downregulated miRNAs [7]
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