ArticleOncology letters2018
Benzo(a)pyrene promotes Hep-G2 cell migration and invasion by upregulating phosphorylated extracellular signal-regulated kinase expression.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Effects of Benzo[a]pyrene on Targeted Therapy Response and Platelet-Activating Factor-Receptor-Mediated Microvesicle Particle Release in Non-Small Cell Lung Cancer.Medical sciences (Basel, Switzerland) · 2026Article
- Curcumin attenuates smoking and drinking activated NF-κB/IL-6 inflammatory signaling axis in cervical cancer.Cancer cell international · 2024Article
- Article
- Article
- Hepatoprotective Effects of Flavonoids against Benzo[a]Pyrene-Induced Oxidative Liver Damage along Its Metabolic Pathways.Antioxidants (Basel, Switzerland) · 2024Review
- Involvement of p38 MAPK pathway in benzo(a)pyrene-induced human hepatoma cell migration and invasion.Environmental science and pollution research international · 2019Article
- Cadmium induces A549 cell migration and invasion by activating ERK.Experimental and therapeutic medicine · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Benzo(a)pyrene (BaP), a carcinogenic component of cigarette smoke, has been reported to activate extracellular signal-regulated kinase (ERK) in cancer cells. Furthermore, activated ERK is associated with liver cancer cell invasion and metastasis. Therefore, the aim of the present study was to investigate the potential role of phosphorylated (p)-ERK in BaP-induced Hep-G2 cell migration and invasion. An MTT assay was used to determine the effects of BaP treatment on Hep-G2 cell proliferation. Wound-healing and Transwell invasion assays were employed to assess the migration and invasion abilities of Hep-G2 cells. Western blot analysis was applied to detect the expression of proteins. The results of the present study demonstrated that BaP treatment was able to increase the level of p-ERK protein expression in Hep-G2 cells. BaP treatment promoted Hep-G2 cell migration and invasion. The ERK inhibitor, U0126, was able to block the migration and invasion abilities of Hep-G2 cells induced by BaP. The results of the present study demonstrated that BaP treatment promoted the migration and invasion of Hep-G2 cells by upregulating p-ERK expression.
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