ArticleBMC gastroenterology2025
Nitidine chloride inhibits colorectal cancer by targeting BUB1: mechanistic insights from molecular dynamics simulation, spatial transcriptomics, and single-cell RNA sequencing.
Article in BMC gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Targeting IGF2BP3 in Cancer: From Molecular Structure and Biology to Early Drug Discovery.International journal of molecular sciences · 2026Review
- CircLRIG1 inhibits the malignant phenotypes of colorectal cancer cells by inactivating the NF-κB signaling through interaction with FUS.Discover oncology · 2026Article
- Article
- BUB1 in cancer genetics and oncogenomics: from chromosomal instability to therapeutic vulnerabilities.Frontiers in genetics · 2026Review
- Nitidine chloride suppresses polo-like kinase 1 via MYCN-associated transcriptional regulation in colorectal cancer: a multi-omics and spatial transcriptomics study.Frontiers in oncology · 2026Article
- Identification and preliminary clinical validation of type 2 diabetes signature genes through machine learning analysis of scRNA-seq data.Frontiers in medicine · 2026Article
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Authors and funding
11 authors.
Funding
Abstract
backgroundColorectal cancer (CRC) is a prevalent malignancy with the efficacy of current treatments limited. Nitidine chloride (NC), a natural alkaloid, exhibits antitumor potential, but its mechanism in CRC remains unclear.
objectiveTo investigate the antitumor effects and mechanisms of NC in CRC for clinical therapeutic strategies.
methodsA Cell Counting Kit-8 was used to assess the viability of HCT116 cells. Xenograft mice received NC (2, 4, 8 mg/kg, intraperitoneal, once every other day for 2 weeks). Transmission electron microscopy and hematoxylin-eosin staining analyzed tumor ultrastructure and pathology. RNA sequencing, real-time quantitative polymerase chain reaction, and molecular dynamics simulation (MDS) examined gene expression and NC-budding uninhibited by benzimidazoles 1 (NC-BUB1) interaction. Single-cell RNA sequencing, spatial transcriptomics, immunohistochemistry, and chromatin immunoprecipitation sequencing explored BUB1 expression and RAD21 regulation. Immune correlation analysis was conducted using TISIDB, TIMER2.0, and deconvolution algorithms (CIBERSORT, CIBERSORT-ABS, EPIC, ESTIMATE, MCPcounter, quanTIseq, TIMER, xCell) to evaluate associations between BUB1 and immune factors or infiltration.
resultsNC inhibited HCT116 cells with time- and concentration-dependent half-maximal inhibitory concentration reduction. NC-treated tumors displayed apoptosis and reduced angiogenesis. Transcriptomics identified BUB1 as a core downregulated gene. Multi-omics confirmed BUB1 overexpression in CRC (1293 vs. 2299 samples; standardized mean difference = 1.77, area under the curve = 0.94) in proliferative/malignant regions. Immune analyses revealed that high BUB1 expression correlated negatively with antigen presentation molecules, chemokines/receptors, and immune cell infiltration (B cells, M2 macrophages, cancer-associated fibroblasts, endothelial cells), suggesting immune microenvironment suppression. BUB1 knockout inhibited CRC cells; NC reduced BUB1 expression. MDS showed a stable NC-BUB1 complex (- 8.8 kcal/mol). The RAD21-BUB1 axis exerted key regulatory roles.
conclusionNC exerts anti-CRC effects by downregulating BUB1, disrupting the RAD21-BUB1 axis, and alleviating BUB1-mediated immune suppression.
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