Colorectal cancer is the third most common malignant tumor worldwide, causing serious harm to human health. Epigenetic modification, especially RNA methylation modification, plays a critical role in the occurrence and development of colorectal cancer via post-transcriptional regulation of mRNA and non-coding RNA expression. Among these, N6-methyladenosine (m⁶A) is the most common chemical modification in mammals, which plays an important role in the progress of cancer, including colorectal cancer. m⁶A is a dynamic and reversible process and is mainly regulated by m⁶A methyltransferase (“writers”), m⁶A demethylases (“erasers”), and m⁶A binding proteins (“readers”). Herein, we reviewed recent advances in the role of m⁶A modification in colorectal cancer and focused on the factors affecting m⁶A modification. Furthermore, we discussed the clinical application of m⁶A modifications for colorectal cancer diagnosis, prognosis, and treatment and provided guides in clinical practice. m⁶A modification and m⁶A regulators play significant roles in the occurrence and development of colorectal cancer by regulating the stability and translation of mRNAs, the maturation of miRNAs, and the function of lncRNAs. m⁶A regulators can play biological roles in colorectal cancer through m⁶A-dependent manner or m⁶A-independent manner. Multiplies of internal factors, including miRNAs and lncRNAs, and external factors can also regulate the m⁶A modification by completing with m⁶A regulators in a base complement manner, regulating the expression of m⁶A and mutating the m⁶A site. m⁶A regulators and m⁶A modificantion are diagnostic and prognostic markers for CRC. Therefore, m⁶A regulators and m⁶A modificantion may be potential therapeutic target for CRC in the future.

Introduction: Imatinib, a tyrosine kinase inhibitor, is the first-line therapy for patients with KIT mutation in gastrointestinal stromal tumor (GIST). Nausea, vomiting, diarrhea, dyspepsia and abdominal pain are common gastrointestinal adverse reactions of imatinib, but imatinib-induced ulcerative colitis (UC) is rarely reported. Case report: We presented a case of UC induced by imatinib in a 56-year-old male patient who experienced this adverse event after 5 years of imatinib 400 mg/d treatment following GIST resection. Management and outcome: The patient's diarrhea and bloody stools showed significant improvement following the discontinuation of imatinib therapy and administration of antidiarrheal medications. Then, imatinib was restarted at a daily dosage of 400 mg. Discussion: UC is a rare adverse event associated with imatinib. Physicians should consider the possibility of UC induced by imatinib when patients present with diarrhea and bloody stool after receiving imatinib treatment. This case offered objective evidence of UC induced by imatinib.