Abstract
Colorectal cancer (CRC) is the third most common cancer and the second leading cause of death due to cancer in the world. Therefore, the identification of novel druggable targets is urgently needed. Tribbles proteins belong to a pseudokinase family, previously recognized in CRC as oncogenes and potential therapeutic targets. Here, we analyzed the expression of TRIB1, TRIB2, and TRIB3 simultaneously in 33 data sets from CRC based on available GEO profiles. We show that all three Tribbles genes are overrepresented in CRC cell lines and primary tumors, though depending on specific features of the CRC samples. Higher expression of TRIB2 in the tumor microenvironment and TRIB3 overexpression in an early stage of CRC development, unveil a potential and unexplored role for these proteins in the context of CRC. Differential Tribbles expression was also explored in diverse cellular experimental conditions where either genetic or pharmacological approaches were used, providing novel hints for future research. This comprehensive bioinformatic analysis provides new insights into Tribbles gene expression and transcript regulation in CRC.
Highlights
Colorectal cancer (CRC) is a carcinoma that develops in the colon or rectum, known as bowel cancer
Different studies have used bioinformatic tools to study the mRNA levels of Tribbles in colorectal cancer (CRC), there are no studies that simultaneously evaluate TRIB1, TRIB2, and TRIB3 gene expression within the same datasets
From a set of CRC samples that included both male and female patients stratified by age at diagnosis, we found that TRIB2, though not TRIB1 nor TRIB3, was preferentially expressed in primary CRC tumors from female patients diagnosed with CRC at an early age (28 to 53 years of age) when compared with patients diagnosed at a later age (69 to 87 years)
Summary
Colorectal cancer (CRC) is a carcinoma that develops in the colon or rectum, known as bowel cancer. The conventional pathway is linked to chromosomal instability (CIN), which refers to a high rate of gains or losses of whole, or large portions of chromosomes, and is observed in 70 to 75% of sporadic CRC [3]. This pathway is characterized by the accumulation of mutations in specific oncogenes, including Epithelial Growth Factor Receptor (EGFR), KRAS proto-oncogene GTPase (KRAS), Cyclooxygenase 2 (COX2), and B-Raf proto-oncogene serine/threonine kinase (BRAF), and tumor suppressor genes, such as Adenomatous Polyposis Coli (APC), Deleted in Colon Cancer (DCC), Phosphatase and Tensin Homolog (PTEN), and Tumor Protein 53 (TP53) [4].
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