ArticleRecent patents on anti-cancer drug discovery2026
Differential Expression and Distribution of Slco4a1 and Slco1b2 in an Internal Environment Disorder-induced Hepatocellular Carcinoma Mouse Model.
Article in Recent patents on anti-cancer drug discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- SLC25A45 as a prognostic biomarker promotes malignant progression via mutant p53 in hepatocellular carcinoma.Journal of gastrointestinal oncology · 2026Article
- Phosphorylation dynamics of sodium-independent organic anion transporter SLCO4A1 and its role in diseases: a review.Frontiers in systems biology · 2026Review
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Authors and funding
4 authors.
Funding
Abstract
objectiveThis study aims to enhance the understanding of underlying mechanisms and potential therapies of the solute carrier organic anion (SLCO) transporter family in internal environment disorder (IED)-induced hepatocellular carcinoma (HCC). This could lead to new therapeutic strategies and offer new directions for the creation of new patents for HCC treatment products.
methodsThe orthotopic transplantation (OT), IED and IED-based OT (IED-OT) mouse models were established. Expression patterns of Slco4a1 and Slco1b2 were determined using reverse transcription quantitative polymerase chain reaction (RT-qPCR), western blotting (WB) and immunohistochemistry (IHC) in various tissues, including lung, stomach, liver, spleen, kidney, colon, small intestine, HCC tissues and adjacent non-cancerous tissues.
resultsAnimals exhibited symptoms, including weight loss, lethargy, chills, dyspnea, altered hair texture, and gastrointestinal disturbances, confirming the successful establishment of the IED model. The analysis demonstrated differential expression and tissue-specific distribution of Slco4a1 and Slco1b2, which are associated with IED-induced changes. These alterations potentially disrupt organ transport functions, thereby promoting the development of HCC. Additionally, they suggest a role in rebalancing the tumor microenvironment and mitigating damage resulting from abnormal substance accumulation. DISCUSSION: This study reveals that IED promotes HCC progression by altering the expression and distribution of Slco4a1 and Slco1b2, leading to transport dysfunction in affected organs. Furthermore, IED and OT exhibit synergistic effects in HCC development. These findings enhance the understanding of the underlying mechanisms of IED related HCC. Future studies should establish animal models incorporating both internal and external factors, with cellular experiments needed to further validate the mechanisms.
conclusionChanges in SLCO expression and distribution induced by IED may play pivotal roles in the development of HCC. These findings contribute insights that could inform novel therapeutic strategies against HCC.
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