ABSTRACT
Colorectal cancer (CRC) is now the third most prevalent tumor and one of the deadliest cancers worldwide, with an increasing prevalence every year. Therefore, we urgently need to understand the mechanisms regulating the progression of colorectal cancer and find potential diagnostic biomarkers. In this study, we performed an analysis using the TCGA and GEO databases to find a molecular biomarker for the diagnosis of CRC, namely CTPS1. The results of this analysis revealed that CTPS1 could promote tumor proliferation and metastasis. Furthermore, bioinformatics analysis revealed that CTPS1 promoted CRC progression through cell cycle and p53 pathways. Further investigation demonstrated that CTPS1 might be involved in the regulation of CCNB1, RRM2, GTSE1, CDK2 and CHEK2 genes. Moreover, PCR confirmed that CTPS1 regulated GTSE1 and CDK2 molecules. Then, western blot was used to verify that CTPS1 promoted the expression of GTSE1 and CDK2 by inhibiting the expression of p53. In summary, we identified an important diagnostic biomarker for CRC, namely CTPS1, and its importance was validated at the cellular level. These results suggest that CTPS1 could serve as a candidate biomarker for CRC and CTPS1 inhibitors may be a potential treatment for CRC.
Declarations
Ethics approval and consent to participate
Not applicable.
Consent for publication
Not applicable.
Availability of data and materials
The datasets generated during and/or analyzed during the current study are available in the [TCGA, GEO] repository.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Authors’ contributions
FH Wu and YD Mao analyzed and interpreted the data, and were major contributor in writing the manuscript. T Ma, XL Wang, HZ Wei, TW Wang and J Wang provided technical support. YC Zhang, who provided ideas and financial support, was our corresponding author. All authors read and approved the final manuscript.
Supplemental data
Supplemental data for this article can be accessed online at https://doi.org/10.1080/15384101.2022.2105084