Mechanism of cinobufacin anti-metastatic colorectal cancer based on integrated mining of proteomics and bioinformatics

Abstract

In this study, the effector proteins of anti-metastatic colorectal cancer (CRC) were mined through proteomics based on the preliminary screening of cinobufacin anti-cancer genes using bioinformatics and the role of cinobufacin anti-metastatic CRC was explored. Proteomics was used to analyze the differential expression of proteins in biopsy tissues of patients with metastatic CRC and bioinformatics was adopted to screen for cinobufacin tumor suppressor genes. The effects of proteomics-mined effector protein CyclinD1 on cell proliferation and colony formation were evaluated by MTT assay and colony formation assay. The cinobufacin sensitivity of metastatic CRC cells were also assessed. After proteomic analysis, the common targets of “Cinobufacin-metastatic CRC” were screened out, among which the tumor-associated CyclinD1 was listed as its level was increased in biopsy tissues of patients with metastatic CRC. The preliminary screening of cinobufacin anti-cancer genes based on bioinformatics found that tumor suppressor gene P53 was closely related to metastatic CRC. CyclinD1 had a relation with P53 mRNA. Further studies showed that P53 was the direct target of CyclinD1 and CyclinD1 overexpression enhanced the sensitivity of metastatic CRC cells to cinobufacin. Using bioinformatics-based gene database analysis technology and proteomics mining technology, the differential expression of proteomics in the biopsy tissues of patients with metastatic CRC and the tumor suppressor genes regulated by cinobufacin were identified. CyclinD1 and P53 found by bioinformatics might be biomarkers for metastatic CRC prognosis, providing a new possible molecular target for anticancer therapy.