ArticleOncogene2022
The NQO1/p53/SREBP1 axis promotes hepatocellular carcinoma progression and metastasis by regulating Snail stability.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 76 citations in OpenAlex.
- Glycolytic reprogramming and the EMT drive cervical cancer progression via the NQO1/HIF1α-SIX1 axis.iScience · 2026Article
- Noninvasive Multi-Omics Radiomic Model Integrating scRNA-seq and Bulk RNA-seq for Hepatocellular Carcinoma Prognosis.Journal of imaging informatics in medicine · 2026Article
- NQO1-Responsive Prodrug for in Cellulo Release of Cytochalasin B as Cancer Cell-Targeted Migrastatic.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- SREBP1 knockdown triggers ferroptosis by suppressing the Nrf2-XCT/GPX4 axis in ovarian cancer.Cell death discovery · 2026Article
- GNPAT promotes immunosuppression in hepatocellular carcinoma by activating the plasmalogen-PPARγ pathway to drive M2 macrophage polarization.Frontiers in immunology · 2026Article
- Targeting MED23 inhibits hepatocellular carcinoma development by suppressing compensatory proliferation and facilitating ROS-mediated cell death.Cell death & disease · 2025Article
- Involvement of KEAP1/NRF2 pathway in non-BRAF mutated squamous cell carcinoma of the thyroid.The Journal of pathology · 2025Article
- Prediction of the effect of Bupleurum chinensis DC. (Chaihu) on survival and its potential targets in hepatocellular carcinoma based on a prognostic model.BMC complementary medicine and therapies · 2025Article
- Herbal Medicine: Enhancing the Anticancer Potential of Natural Products in Hepatocellular Carcinoma Therapy Through Advanced Drug Delivery Systems.Pharmaceutics · 2025Review
- CPT1A/HIF-1α positive feedback loop induced fatty acid oxidation metabolic pathway contributes to the L-ascorbic acid-driven angiogenesis in breast cancer.Breast cancer research : BCR · 2025Article
- The Role of Cholesterol Metabolism and Its Regulation in Tumor Development.Cancer medicine · 2025Review
- Computational modelling identifies primary mediators of crosstalk between DNA damage and oxidative stress responses.PLoS computational biology · 2025Article
- miR-485-5p/NQO1 axis drives colorectal cancer progression by regulating apoptosis and aerobic glycolysis.Cancer cell international · 2025Article
- CCDC154 knockdown inhibits growth of liver cancer via suppressing expression of Snail.European journal of medical research · 2025Article
- Clinical Significance of a Novel Vasculogenic Mimicry-based Prognostic Model in Hepatocellular Carcinoma.Current medicinal chemistry · 2025Article
- Racial disparities in hepatocellular carcinoma: a TCGA-based gene expression study of Caucasian and Asian populations.Exploration of targeted anti-tumor therapy · 2025Article
- BTF3 affects hepatocellular carcinoma progression by transcriptionally upregulating PDCD2L and inactivating p53 signaling.Molecular medicine (Cambridge, Mass.) · 2024Article
- Role of ATP citrate lyase and its complementary partner on fatty acid synthesis in gastric cancer.Scientific reports · 2024Article
- From regulation to deregulation of p53 in hematologic malignancies: implications for diagnosis, prognosis and therapy.Biomarker research · 2024Review
- Aurantio‑obtusin regulates lipogenesis and ferroptosis of liver cancer cells through inhibiting SCD1 and sensitizing RSL3.International journal of oncology · 2024Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related mortality worldwide, and its abnormal metabolism affects the survival and prognosis of patients. Recent studies have found that NAD(P)H quinone oxidoreductase-1 (NQO1) played an important role in tumor metabolism and malignant progression. However, the molecular mechanisms by which NQO1 regulates lipid metabolism during HCC progression remain unclear. In this study, bioinformatics analysis and immunohistochemical results showed that NQO1 was highly expressed in HCC tissues and its high expression was closely related to the poor prognosis of HCC patients. Overexpression of NQO1 promoted the cell proliferation, epithelial-to-mesenchymal transition (EMT) process, and angiogenesis of HCC cells. Luciferase reporter assay further revealed that NQO1/p53 could induce the transcriptional activity of SREBP1, consequently regulating HCC progression through lipid anabolism. In addition, Snail protein was stabilized by NQO1/p53/SREBP1 axis and triggered the EMT process, and participated in the regulatory role of NQO1/p53/SREBP1 axis in HCC. Together, these data indicated that NQO1/SREBP1 axis promoted the progression and metastasis of HCC, and might be a potential therapeutic target for HCC.
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