ArticleCancer management and research2019
TINAGL1 promotes hepatocellular carcinogenesis through the activation of TGF-β signaling-medicated VEGF expression.
Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 41 citations in OpenAlex.
- Placental molecular subtypes of severe preeclampsia reveal divergent aging trajectories and fetal growth outcomes.medRxiv : the preprint server for health sciences · 2026Article
- Mesenteric adipose-derived exosomal TINAGL1 enhances intestinal fibrosis in Crohn's Disease via SMAD4.Journal of advanced research · 2025Article
- Tubulointerstitial nephritis antigen-like 1 promotes the progression of liver fibrosis after HCV eradication with direct-acting antivirals.International journal of biological sciences · 2025Article
- Implications of ZNF334 gene in lymph node metastasis of lung SCC: potential bypassing of cellular senescence.Journal of translational medicine · 2024Article
- Tubulointerstitial nephritis antigen-like 1 from cancer-associated fibroblasts contribute to the progression of diffuse-type gastric cancers through the interaction with integrin β1.Journal of translational medicine · 2024Article
- Tubulointerstitial nephritis antigen-like 1 is a novel matricellular protein that promotes gastric bacterial colonization and gastritis in the setting of Helicobacter pylori infection.Cellular & molecular immunology · 2023Article
- Low TINAGL1 expression is a marker for poor prognosis in breast cancer.Journal of cancer research and clinical oncology · 2023Article
- Lipocalin family proteins and their diverse roles in cardiovascular disease.Pharmacology & therapeutics · 2023Review
- Construction and validation of a tumor mutational burden and immune-related prognostic model for predicting the prognosis of patients with lung squamous cell carcinoma.Journal of thoracic disease · 2023Article
- First Characterization of the Transcriptome of Lung Fibroblasts of SSc Patients and Healthy Donors of African Ancestry.International journal of molecular sciences · 2023Article
- Recent progress in molecular mechanisms of postoperative recurrence and metastasis of hepatocellular carcinoma.World journal of gastroenterology · 2022Review
- Ancestry-dependent gene expression correlates with reprogramming to pluripotency and multiple dynamic biological processes.Science advances · 2020Article
- Inhibitory effect of dihydromyricetin on the proliferation of JAR cells and its mechanism of action.Oncology letters · 2020Article
- Tubulointerstitial nephritis antigen-like 1 deficiency alleviates age-dependent depressed ovulation associated with ovarian collagen deposition in mice.Reproductive medicine and biology · 2020Article
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5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeTubulointerstitial nephritis antigen-like 1 (TINAGL1) is an extracellular matrix protein that plays an important role in cell adhesion and therefore modulates cell proliferation, migration, and differentiation. In addition, it is frequently upregulated in highly metastatic tumors. The aim of our study was to determine the role of TINAGL1 in the progression and metastasis of hepatocellular carcinoma (HCC). MATERIALS AND
methodsTINAGL1 mRNA levels were analyzed in HCC and adjacent non-tumorous samples by reverse transcription polymerase chain reaction (RT-PCR). Human HCC cell lines were transfected with lentiviral plasmids expressing either si-TINAGL1 or TINAGL1 and subjected to CCK-8, colony forming, transwell migration, Annexin V/propidium iodide, and 5-ethynyl-2'-deoxyuridine uptake assays. Suitably transfected HCC cells were injected into athymic nude mice to establish xenograft tumors that were imaged and measured on a weekly basis. Mediators of the TGF-β signaling pathway were analyzed by Western blot.
resultsTINAGL1 was upregulated in human HCC tissues and associated with poor prognosis. TINAGL1 knockdown suppressed HCC cell growth, proliferation, and migration and induced apoptosis in HCC cells, whereas TINAGL1 overexpression had opposite effects. In addition, inhibition of TINAGL1 retarded xenograft tumor growth in a nude mouse model. Mechanistically, TINAGL1 activated the TGF-β signaling pathway and increased VEGF secretion.
conclusionTINAGL1 promotes hepatocellular carcinogenesis and metastasis via the TGF-β/Smad3/VEGF axis and is a potential new biomarker of HCC.
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