ArticleBMC cancer2023
ARL4C is associated with epithelial-to-mesenchymal transition in colorectal cancer.
Article in BMC cancer, 2023. 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, 8 citations in OpenAlex.
- Implications of ADP-Ribosylation Factor-Like Protein 4C (ARL4C) in Human Neoplasia With Special Emphasis on Ameloblastoma: A Scoping Review.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2026Article
- Identification of M2 macrophage-related biomarkers for a predictive model of interstitial fibrosis and tubular atrophy after kidney transplantation by machine learning algorithms.Translational andrology and urology · 2025Article
- Integrated lncRNA and mRNA analysis reveals the immune modulatory mechanisms of antimicrobial peptide BSN-37 in mouse peritoneal macrophages.Scientific reports · 2025Article
- Ursolic acid in colorectal cancer: mechanisms, current status, challenges, and future research directions.Pharmacological reports : PR · 2025Review
- Ursolic acid inhibits the metastasis of colon cancer by downregulating ARL4C expression.Oncology reports · 2024Article
- Prognostic stratification of sepsis through DNA damage response based RiskScore system: insights from single-cell RNA-sequencing and transcriptomic profiling.Frontiers in immunology · 2024Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundADP-ribosylation factor-like protein 4 C (ARL4C) is a member of the ARF small GTP-binding protein subfamily. The ARL4C gene is highly expressed in colorectal cancer (CRC). ARL4C protein promotes cell motility, invasion, and proliferation.
methodsWe investigated the characteristics of ARL4C by comparing its expression at the invasion front and relationships with clinicopathological data using RNAscope, a highly sensitive RNA in situ method.
resultsIn all cases, ARL4C expression was observed in cancer stromal cells and cancer cells. ARL4C expression in cancer cells was localized at the invasion front. In cancer stromal cells, ARL4C expression was significantly stronger in cases with high-grade tumor budding than in cases with low-grade tumor budding (P = 0.0002). Additionally, ARL4C expression was significantly increased in patients with high histological grade compared with those with low histological grade (P = 0.0227). Furthermore, ARL4C expression was significantly stronger in lesions with the epithelial-to-mesenchymal transition (EMT) phenotype compared with the non-EMT phenotype (P = 0.0289). In CRC cells, ARL4C expression was significantly stronger in cells that had the EMT phenotype compared with those with a non-EMT phenotype (P = 0.0366). ARL4C expression was significantly higher in cancer stromal cells than in CRC cells (P < 0.0001).
conclusionOur analysis reinforces the possibility that ARL4C expression worsens the prognosis of patients with CRC. Further elucidation of the function of ARL4C is desired.
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