Benzo[a]pyrene-induced cell cycle progression occurs via ERK-induced Chk1 pathway activation in human lung cancer cells

Wang, Bing‐Yen; Wu, Sung–Yu; Tang, Sheau‐Chung; Lai, Chintu; Ou, Chu‐Chyn; Wu, Ming‐Fang; Hsiao, Yi‐Min; Ko, Jiunn‐Liang

doi:10.1016/j.mrfmmm.2015.01.009

Cited by 17 publications

(6 citation statements)

References 23 publications

(27 reference statements)

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“…Neither PCB180 nor 3'-OH-PCB180 phosphorylated p53 Ser15 under our in vitro experimental conditions (data not shown). BaP, on the other hand, increased p53 Ser15 levels time dependently (data not shown), which is in line with previous work (Darzynkiewicz, Traganos et al 2011, Loughery, Cox et al 2014, Wang, Wu et al 2015. PCB180 did not induce γH2AX at any time point (Fig.…”

Section: In Vitro Induction Of Genotoxic Stress By Pcb180 and Its Metsupporting

confidence: 92%

Hydroxyl metabolite of PCB 180 induces DNA damage signaling and enhances the DNA damaging effect of benzo[a]pyrene

Al-Anati

Viluksela

Strid

et al. 2015

Chemico-Biological Interactions

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Section: In Vitro Induction Of Genotoxic Stress By Pcb180 and Its Metsupporting

confidence: 92%

Hydroxyl metabolite of PCB 180 induces DNA damage signaling and enhances the DNA damaging effect of benzo[a]pyrene

Al-Anati

Viluksela

Strid

et al. 2015

Chemico-Biological Interactions

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“…It activates several types of cancer, mainly by causing DNA damage through BPDE-DNA adduct and ROS formation [41,42]. Unfortunately, we are constantly exposed to low-doses of B[a]P, which induces cancer in the body through its conversion to the BPDE metabolite [43,44]. Research on the protective effects of natural compounds against B[a]P-induced damage is currently ongoing to identify methods to prevent cancer [45][46][47][48][49].…”

Section: Discussionmentioning

confidence: 99%

Modulatory Effects of Silymarin on Benzo[a]pyrene-Induced Hepatotoxicity

Jee

Kim

Sung

2020

IJMS

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Benzo[a]pyrene (B[a]P), a polycyclic aromatic hydrocarbon, is a group 1 carcinogen that introduces mutagenic DNA adducts into the genome. In this study, we investigated the molecular mechanisms underlying the involvement of silymarin in the reduction of DNA adduct formation by B[a]P-7,8-dihydrodiol-9,10-epoxide (BPDE), induced by B[a]P. B[a]P exhibited toxicity in HepG2 cells, whereas co-treatment of the cells with B[a]P and silymarin reduced the formation of BPDE-DNA adducts, thereby increasing cell viability. Determination of the level of major B[a]P metabolites in the treated cells showed that BPDE levels were reduced by silymarin. Nuclear factor erythroid 2-related factor 2 (Nrf2) and pregnane X receptor (PXR) were found to be involved in the activation of detoxifying genes against B[a]P-mediated toxicity. Silymarin did not increase the expression of these major transcription factors, but greatly facilitated their nuclear translocation. In this manner, treatment of HepG2 cells with silymarin modulated detoxification enzymes through NRF2 and PXR to eliminate B[a]P metabolites. Knockdown of Nrf2 abolished the preventive effect of silymarin on BPDE-DNA adduct formation, indicating that activation of the Nrf2 pathway plays a key role in preventing B[a]P-induced genotoxicity. Our results suggest that silymarin has anti-genotoxic effects, as it prevents BPDE-DNA adduct formation by modulating the Nrf2 and PXR signaling pathways.

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“…For example, Patten Hitt et al ( 41 ) demonstrated that BaP activated ERK, which was involved in cell proliferation, in colon adenocarcinoma HT29 cells ( 41 ). Wang et al ( 42 ) reported that BaP-induced cell cycle progression occurred via the ERK-induced checkpoint kinase 1 pathway activation in human lung cancer cells. Kometani et al ( 43 ) reported that the EGFR tyrosine kinase inhibitor reduced the cellular proliferation and the level of phosphorylation of ERK1/2, which is a downstream signal of the EGFR in BaP-treated A549 cells.…”

Section: Discussionmentioning

confidence: 99%

Benzo(a)pyrene promotes Hep‑G2 cell migration and invasion by upregulating phosphorylated extracellular signal‑regulated kinase expression

Wang

Pan

et al. 2018

Oncol Lett

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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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Benzo[a]pyrene-induced cell cycle progression occurs via ERK-induced Chk1 pathway activation in human lung cancer cells

Cited by 17 publications

References 23 publications

Hydroxyl metabolite of PCB 180 induces DNA damage signaling and enhances the DNA damaging effect of benzo[a]pyrene

Hydroxyl metabolite of PCB 180 induces DNA damage signaling and enhances the DNA damaging effect of benzo[a]pyrene

Modulatory Effects of Silymarin on Benzo[a]pyrene-Induced Hepatotoxicity

Benzo(a)pyrene promotes Hep‑G2 cell migration and invasion by upregulating phosphorylated extracellular signal‑regulated kinase expression

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