Journal
BIOLOGY-BASEL
Volume 10, Issue 6, Pages -Publisher
MDPI
DOI: 10.3390/biology10060500
Keywords
rectal cancer; radiation therapy; radio-responsiveness; bio-marker; DNA methylation
Categories
Funding
- Korea Institute of Radiological and Medical Sciences (KIRAMS) - Ministry of Science, ICT and Future Planning, Republic of Korea [50337-2021, 50531-2021, 50542-2021]
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The standard treatment for locally advanced rectal cancer (LARC) involves chemotherapy, radiotherapy, and surgery. Identifying biomarkers that can discriminate radio-responsiveness before surgery is crucial to improve treatment outcomes and reduce side effects. Research has identified candidate genes involved in radio-responsiveness, such as CTSE, which exhibited differential methylation at the promoter region inversely correlated with radio-resistance. This study aims to develop a gene chip for diagnosing radio-responsiveness in LARC patients, with the potential to improve patient prognosis.
Simple Summary Standard treatment of locally advanced rectal cancer (LARC) consists of chemotherapy, radiotherapy, and surgery. Identification of radio-resistant (RR) and radio-sensitive (RS) LARC has been a major hurdle for patient-specific treatment. The development of biomarkers that can discriminate radio-responsiveness before surgery could improve standard treatment and minimize unwanted side effects. LARC patients were sorted according to their radio-responsiveness and patient-derived organoids were established from the respective cancer tissues. Expression profiles for each group were obtained using RNA-seq. Biological and bioinformatic analysis approaches were used in deciphering genes and pathways that participate in the radio-resistance of LARC. Thirty candidate genes encoding proteins involved in radio-responsiveness-related pathways, including the immune system, DNA repair and cell-cycle control, were identified. Interestingly, one of the candidate genes, cathepsin E (CTSE), exhibited differential methylation at the promoter region that was inversely correlated with the radio-resistance of patient-derived organoids, suggesting that methylation status could contribute to radio-responsiveness. On the basis of these results, we plan to pursue development of a gene chip for diagnosing the radio-responsiveness of LARC patients, with the hope that our efforts will ultimately improve the prognosis of LARC patients.
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