ArticleCell death & disease2023
Involvement and targeted intervention of benzo(a)pyrene-regulated apoptosis related proteome modification and muti-drug resistance in hepatocellular carcinoma.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 27 citations in OpenAlex.
- Transcriptomic Analysis Reveals Core Genes and Mechanisms Linking Grilled Food Toxicants (4-HNE, BaP, PhIP) to NASH-HCC Progression.Food science & nutrition · 2026Article
- A cigarette compound-induced tumor microenvironment promotes sorafenib resistance in hepatocellular carcinoma via the 14-3-3η-modified tumor-associated proteome.Chinese medical journal · 2026Article
- Mechanisms and targeted prevention of abnormal ductular reaction caused by a low concentration of Benzo(a)pyrene.Cell death & disease · 2025Article
- Environmental Pollutants, Occupational Exposures, and Liver Disease.Seminars in liver disease · 2025Review
- Article
- Adjuvant Properties of Caffeic Acid in Cancer Treatment.International journal of molecular sciences · 2024Review
- Effective therapy of advanced breast cancer through synergistic anticancer by paclitaxel and P-glycoprotein inhibitor.Materials today. Bio · 2024Article
- Mitophagy and clear cell renal cell carcinoma: insights from single-cell and spatial transcriptomics analysis.Frontiers in immunology · 2024Article
- Unraveling the molecular links between benzopyrene exposure, NASH, and HCC: an integrated bioinformatics and experimental study.Scientific reports · 2023Article
- Azadirachtin Attenuates Carcinogen Benzo(a) Pyrene-Induced DNA Damage, Cell Cycle Arrest, Apoptosis, Inflammatory, Metabolic, and Oxidative Stress in HepG2 Cells.Antioxidants (Basel, Switzerland) · 2023Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During the development of hepatocellular carcinoma (HCC), the mutual adaptation and interaction of HCC cells and the microenvironment play an important role. Benzo(a)pyrene (B[a]P) is a common environmental pollutant, which can induce the initiation of various malignant tumors, including HCC. However, the effects of B[a]P exposure on progression of HCC and the potential mechanisms remains largely uninvestigated. Here we found that, after the long-term exposure of HCC cells to low dose of B[a]P, it activated glucose-regulated protein 75 (GRP75), which then induced a modification of apoptosis-related proteome. Among them, we identified the X-linked inhibitor of apoptosis protein (XIAP) as a key downstream factor. XIAP further blocked the caspase cascade activation and promoted the acquisition of the anti-apoptosis abilities, ultimately leading to multi-drug resistance (MDR) in HCC. Furthermore, the abovementioned effects were markedly attenuated when we inhibited GRP75 by using 3,4-dihydroxycinnamic acid (caffeic acid, CaA). Collectively, our present study revealed the effects of B[a]P exposure on the progression of HCC, and identified GRP75 was a meaningful factor involved in.
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