ArticleCancer cell international2020
LncRNA FTX represses the progression of non-alcoholic fatty liver disease to hepatocellular carcinoma via regulating the M1/M2 polarization of Kupffer cells.
Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- LncRNA and circRNA in Patients with Non-Alcoholic Fatty Liver Disease: A Systematic Review.Biomolecules · 2023Pooled it
- The role of liver macrophages in viral liver pathogenesis.Journal of leukocyte biology · 2025Review
- Investigating the Diagnostic Utility of LncRNA GAS5 in NAFLD Patients.Biomedicines · 2025Article
- LncRNA FTX promotes colorectal cancer radioresistance through disturbing redox balance and inhibiting ferroptosisWorld journal of gastroenterology · 2025Article
- Glycolysis-related lncRNA FTX upregulates YAP1 to facilitate colorectal cancer progression via sponging miR-215-3p.Scientific reports · 2025Article
- Comprehensive review of macrophage models: primary cells and immortalized lines across species.Frontiers in immunology · 2025Review
- Novel regulators of hepatic macrophages in liver fibrosis.Frontiers in immunology · 2025Review
- LncRNA FTX accelerates the progression of hepatocellular carcinoma by FTX/miR-374a-3p/HMGB1 pathway.International journal of medical sciences · 2025Article
- Mechanistic role of long non-coding RNAs in the pathogenesis of metabolic dysfunction-associated steatotic liver disease and fibrosis.eGastroenterology · 2024Article
- Epigenetic modifications in obesity-associated diseases.MedComm · 2024Review
- Long Non-coding RNAs Regulating Macrophage Polarization in Liver Cancer.Current pharmaceutical design · 2024Review
- Communication molecules (ncRNAs) mediate tumor-associated macrophage polarization and tumor progression.Frontiers in cell and developmental biology · 2024Review
- Review
- Tumour-associated macrophages: versatile players in the tumour microenvironment.Frontiers in cell and developmental biology · 2023Review
- LINC01468 drives NAFLD-HCC progression through CUL4A-linked degradation of SHIP2.Cell death discovery · 2022Article
- The Implications of Noncoding RNAs in the Evolution and Progression of Nonalcoholic Fatty Liver Disease (NAFLD)-Related HCC.International journal of molecular sciences · 2022Review
- Noncoding RNA-mediated molecular bases of chemotherapy resistance in hepatocellular carcinoma.Cancer cell international · 2022Review
- Long non-coding RNA GAS5 contributes to the progression of nonalcoholic fatty liver disease by targeting the microRNA-29a-3p/NOTCH2 axis.Bioengineered · 2022Article
- Distinct hepatic immunological patterns are associated with the progression or inhibition of hepatocellular carcinoma.Cell reports · 2022Article
- Resident Immune Cells of the Liver in the Tumor Microenvironment.Frontiers in oncology · 2022Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe effect of lncRNA FTX on non-alcoholic fatty liver disease (NAFLD) conversion to hepatocellular carcinoma (HCC) is unclear.
methodsIn our study, C57BL/6 mice was fed with high fat diet for obtaining NAFLD mouse model, and diethylnitrosamine induced the formation of HCC tumor. The expression of iNOS and CD206 in tissues were examined using immunohistochemistry. In addition, qRT-PCR was implemented to detect the expression of FTX and mRNAs. The percentage of M1 and M2 Kupffer cells (KCs) were determined using flow cytometry. The pathological change in liver tissues was displayed by H&E staining. Besides, immunofluorescence assay was performed to ensure the primary KCs through labeling F4/80.
resultsHere, we found that the expression of FTX and the ratio of M1/M2 KCs in liver tissues from NAFLD-transformed HCC (NAFLD-HCC) patients lower than in liver tissues from NAFLD patients. Subsequently, we revealed that the expression of FTX and M1/M2 KCs ratio were downregulated during NAFLD conversion to HCC. Importantly, increasing of FTX inhibited HCC tumor growth, improved liver damage and promoted M1 polarization of KCs during NAFLD conversion to HCC, while these effects of FTX were reversed by inactivating of KCs. Finally, in vitro experiments, our data indicated that FTX facilitated the M1 polarization of KCs.
conclusionIn conclusion, our results demonstrated that upregulation of FTX suppressed NAFLD conversion to HCC though promoting M1 polarization of KCs. Our findings presented a new regulatory mechanism for NAFLD conversion to HCC, and provided a new biomarker for inhibiting this conversion.
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