Abstract
The occurrence and development of colorectal cancer (CRC) is strongly associated with mutations, deletions, or microsatellite instability (MSI) of specific genes. Accurate and efficient detection of these molecular gene markers allows for rapid risk assessment and treatment options for diseased individuals. Polymerase chain reaction (PCR) and DNA gel electrophoresis, as mature, basic and relatively economical core technologies of molecular biology, play an important role in gene variation analysis. According to this, PCR and gel electrophoresis technology may become the main means of detecting colorectal cancer in the future. So, the purpose of this study was to systematically explore the combined application strategy of PCR technology and DNA gel electrophoresis in the detection of key gene (SETD2) variants in colorectal cancer through three mouse models (SETD2-flox mouse, SETD2/Villin-creER mouse, wild type mouse). In summary, the combined application of PCR and DNA gel electrophoresis provides a simple, low-cost, cost-effective intuitive and reliable method for molecular analysis of colorectal cancer. By efficiently identifying key gene variants and directly guiding clinical drug decisions, it has important practical value for promoting the popularity of precision diagnosis and further treatment of colorectal cancer, improving patient prognosis and future scientific research.
References
[1] Housini M, Dariya B, Ahmed N, et al. Colorectal cancer: Genetic alterations, novel biomarkers, current therapeutic strategies and clinical trials. Gene. 2024;892:147857.
[2] Dee EC, Laversanne M, Bhoo-Pathy N, et al. Cancer incidence and mortality estimates in 2022 in southeast Asia: a comparative analysis. Lancet Oncol. 2025;26(4):516-528.
[3] Bürtin F, Mullins CS, Linnebacher M. Mouse models of colorectal cancer: Past, present and future perspectives. World J Gastro-enterol. 2020 Apr 7;26(13):1394-426.
[4] Ma C, Liu M, Feng W, Rao H, Zhang W, Liu C, Xu Y, Wang Z, Teng Y, Yang X, Ni L, Xu J, Gao WQ, Lu B, Li L. Loss of SETD2 aggravates colorectal cancer progression caused by SMAD4 deletion through the RAS/ERK signalling pathway. Clin Transl Med. 2023 Nov;13(11):e1475.
[5] Canene-Adams K. General PCR. Methods Enzymol. 2013;529:291-8.
[6] Hanada K. Introduction and Perspectives of DNA Electrophoresis. Methods Mol Biol. 2020;2119:1-13.
[7] Yuan H, Li N, Fu D, Ren J, Hui J, Peng J, Liu Y, Qiu T, Jiang M, Pan Q, Han Y, Wang X, Li Q, Qin J. Histone methyltransferase SETD2 modulates alternative splicing to inhibit intestinal tumorigenesis. J Clin Invest. 2017 Sep 1;127(9):3375-91.
[8] Philip PA, Azar I, Xiu J, Hall MJ, Hendifar AE, Lou E, Hwang JJ, Gong J, Feldman R, Ellis M, Stafford P, Spetzler D, Khush-man MM, Sohal D, Lockhart AC, Weinberg BA, El-Deiry WS, Marshall J, Shields AF, Korn WM. Molecular Characterization of KRAS Wild-type Tumors in Patients with Pancreatic Adenocarcinoma. Clin Cancer Res. 2022 Jun 13;28(12):2704-14.