Published online Apr 15, 2024. doi: 10.4251/wjgo.v16.i4.1453
Peer-review started: December 5, 2023
First decision: December 18, 2023
Revised: December 31, 2023
Accepted: February 2, 2024
Article in press: February 2, 2024
Published online: April 15, 2024
Processing time: 127 Days and 19.5 Hours
Radiotherapy stands as a promising therapeutic modality for colorectal cancer (CRC); yet, the formidable challenge posed by radio-resistance significantly undermines its efficacy in achieving CRC remission.
Radiotherapy can effectively inhibit the proliferation of cancer cells, but a considerable number of CRC patients are still resistant to radiotherapy, and further exploration of potential drug resistance targets is needed to provide a theoretical basis for developing effective treatment strategies to improve response rate.
To analyze the role of microRNA-298 (miR-298) in the radioresistance of CRC and its molecular mechanism. MiRNAs are involved in a wide range of physiological and pathological processes, and the dysregulation of miR-298 has been shown to be related to the development of CRC. However, the exact role that miR-298 plays in the radioresistance of CRC cells remains to be elucidated.
This study established a radiation-resistant CRC cell line, which exposes HT-29 cells to 5 gray ionizing radiation, followed by a 7-d recovery period. The miR-298 expression level and the biological behavior of HT-29 cells were examined before and after radiotherapy. To explore the radiosensitivity and the expression of downstream target genes in ectopic CRC model tumors after overexpressing miR-298. Dual-luciferase reporter assay for the binding site of DYRK1A with miR-298. Knockdown of miR-298 observed DYRK1A expression and radiation-induced apoptosis were improved in HT-29 cells.
We observed a significant upregulation of miR-298 in radioresistant CRC cells. MiR-298 emerged as a key determinant of cell survival after radiation exposure, as its overexpression resulted in a significant reduction in radiation-induced apoptosis. Interestingly, there was a strong correlation between miR-298 expression and CRC cell viability. Further studies revealed DYRK1A as a direct target of miR-298. Taken together, our results highlight the role that miR-298 plays in enhancing radioresistance in CRC cells by downregulation of DYRK1A, thereby positioning miR-298 as a promising candidate gene.
This study revealed an important target of CRC resistance to radiotherapy, miR-298, an effect of DYRK1A to enhance radioresistance in CRC cells. This study provides proof of principle for the development of a protocol based on radiotherapy + targeting for CRC.
Cancer radiotherapy resistance remains a major challenge for cancer patients. To improve patient outcomes, we need to further understand the mechanisms by which tumor ecosystem tumor cell proliferation, apoptosis, invasion, and migration under the induction of continuous therapy. Analysis of the targets of radiotherapy sensitive/resistant to tumors will help to discover new therapeutic opportunities.