Gene Technology

Targeting DDX18 for Chemotherapy Sensitization: A Strategy for Colorectal Cancer Treatment

Charlotte Taylor^* Department of Biotechnology, University of Edinburgh, Edinburgh, United Kingdom
^*Correspondence: Charlotte Taylor, Department of Biotechnology, University of Edinburgh, Edinburgh, United Kingdom, Email:

Received: 29-Nov-2024, Manuscript No. RDT-24-28172; Editor assigned: 02-Dec-2024, Pre QC No. RDT-24-28172 (PQ); Reviewed: 16-Dec-2024, QC No. RDT-24-28172; Revised: 23-Dec-2024, Manuscript No. RDT-24-28172 (R); Published: 30-Dec-2024, DOI: 10.35248/2329-6682.24.13.298

Description

The study of how genetic factors influence the response of cancer cells to chemotherapy is critical for advancing treatment strategies. One such factor, DEAD-box RNA helicase 18 (DDX18), has recently proven as a key player in regulating chemotherapy sensitivity in Colorectal Cancer (CRC) through its role in maintaining genomic stability. Colorectal cancer remains one of the most common and deadly malignancies worldwide and despite advances in chemotherapy, the development of drug resistance continues to be a major obstacle in the treatment of CRC. Understanding the mechanisms that control chemotherapy sensitivity is essential for improving therapeutic outcomes and DDX18 appears to be an important factor in this process.

DDX18 is a member of the DEAD-box RNA helicase family, proteins known for their involvement in RNA metabolism and the regulation of various cellular processes, including translation, splicing and RNA decay. Recent research has uncovered a novel function for DDX18 in regulating genomic stability, a critical aspect of cellular function. In CRC, DDX18 is thought to contribute to maintaining the integrity of the genome, preventing DNA damage accumulation and ensuring proper cell division. This is especially important in the context of chemotherapy, where DNA-damaging agents are used to reduce rapidly dividing cancer cells. When the integrity of the genome is compromised, cancer cells may become resistant to chemotherapy, leading to treatment failure.

The regulation of genomic stability by DDX18 is particularly relevant in CRC because this cancer is often associated with mutations in key genes that control cell cycle progression and DNA repair pathways. These mutations can lead to genomic instability, a characteristic feature of cancer that allows tumor cells to accumulate additional genetic alterations, some of which may contribute to resistance to chemotherapy. By stabilizing the genome and preventing excessive DNA damage, DDX18 helps to ensure that cancer cells remain sensitive to chemotherapy-induced cell death. This makes DDX18 an attractive target for therapeutic strategies aimed at overcoming chemotherapy resistance in CRC.

Recent studies have highlighted the potential of targeting DDX18 as a way to sensitize CRC cells to chemotherapy. By enhancing the expression or activity of DDX18, it may be possible to restore genomic stability in cancer cells, thereby preventing the development of resistance mechanisms. This could improve the effectiveness of chemotherapy in patients who have developed resistance to standard treatments. Additionally, DDX18 may serve as a useful biomarker for predicting chemotherapy sensitivity in CRC patients. Patients whose tumors have high levels of DDX18 expression may be more likely to respond to chemotherapy, whereas those with low levels of DDX18 may require alternative therapeutic approaches.

The involvement of DDX18 in regulating genomic stability also highlights the broader importance of RNA helicases in cancer biology. RNA helicases, including DDX18, are critical for maintaining proper cellular function and genomic integrity. Their role in regulating DNA repair, cell cycle progression and response to DNA damage suggests that they could be targeted for therapeutic intervention in a wide range of cancers, not just CRC. Targeting RNA helicases like DDX18 could potentially offer an innovative approach to cancer therapy, especially for patients with tumors that are resistant to traditional chemotherapy drugs.

In conclusion, DDX18 represents an exciting new target for overcoming chemotherapy resistance in colorectal cancer by regulating genomic stability. Its role in maintaining DNA integrity makes it a key factor in ensuring that cancer cells remain sensitive to chemotherapy-induced damage. Further research is needed to fully elucidate the mechanisms by which DDX18 influences chemotherapy sensitivity, but the potential for targeting this protein as part of a therapeutic strategy holds promise for improving outcomes in CRC patients. As our understanding of DDX18’s function continues to evolve, it could become an important tool in the fight against chemotherapy resistance and help to create the path for more effective treatments for colorectal cancer and other malignancies.