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ZnO nanoparticles promote the malignant transformation of colorectal epithelial cells in APCmin/+ mice
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Highlights ZnO NPs induce chronic inflammation in colorectal mucosal epithelia. ZnO NPs promote malignant transformation of colonic cells in APCmin/+ mice. ZnO NPs promote tumorigenesis through activating CXCR2. Free-zinc release of ZnO NPs promotes the malignant transformation.
Abstract As the use of zinc oxide nanoparticles (ZnO NPs) in everyday products grows, so does concern about health risks. However, no findings on the gastrointestinal toxicity of ZnO NPs have been published. We investigated the possible malignant transformation of ZnO NPs in the mice’s colonic tissues using the APCmin/+ mouse model with a premalignant lesion in intestinal epithelial cells. Higher doses and long-term oral exposure to ZnO NPs were found to mildly promote colonic inflammation in WT mice, while they moderately or strongly exacerbated the severity of chronic inflammation and tumorigenesis in APCmin/+ mice with intestinal adenomatous polyposis. The ZnO NPs-induced inflammation and tumorigenesis in colonic epithelial cells was linked to the activation of CXCR2/NF-κB/STAT3/ERK and AKT pathways. Analysis of the ZnO NPs-exacerbated intestinal adenomatous polyposis in APCmin/+ mice revealed that ZnO NPs could activate the APC-driven Wnt/β-catenin signaling pathway, exacerbating intestinal tumorigenesis. In fact, ZnO NPs have been shown to increase intestinal inflammation and tumorigenesis in APCmin/+ mice by releasing free Zn2+. In WT mice, a low dose of ZnO NPs (26 mg/kg/day) did not cause intestinal inflammation. In conclusion, higher doses and prolonged exposure to ZnO NPs promote the malignant transformation of precancerous epithelial cells.
ZnO nanoparticles promote the malignant transformation of colorectal epithelial cells in APCmin/+ mice
Graphical abstract Display Omitted
Highlights ZnO NPs induce chronic inflammation in colorectal mucosal epithelia. ZnO NPs promote malignant transformation of colonic cells in APCmin/+ mice. ZnO NPs promote tumorigenesis through activating CXCR2. Free-zinc release of ZnO NPs promotes the malignant transformation.
Abstract As the use of zinc oxide nanoparticles (ZnO NPs) in everyday products grows, so does concern about health risks. However, no findings on the gastrointestinal toxicity of ZnO NPs have been published. We investigated the possible malignant transformation of ZnO NPs in the mice’s colonic tissues using the APCmin/+ mouse model with a premalignant lesion in intestinal epithelial cells. Higher doses and long-term oral exposure to ZnO NPs were found to mildly promote colonic inflammation in WT mice, while they moderately or strongly exacerbated the severity of chronic inflammation and tumorigenesis in APCmin/+ mice with intestinal adenomatous polyposis. The ZnO NPs-induced inflammation and tumorigenesis in colonic epithelial cells was linked to the activation of CXCR2/NF-κB/STAT3/ERK and AKT pathways. Analysis of the ZnO NPs-exacerbated intestinal adenomatous polyposis in APCmin/+ mice revealed that ZnO NPs could activate the APC-driven Wnt/β-catenin signaling pathway, exacerbating intestinal tumorigenesis. In fact, ZnO NPs have been shown to increase intestinal inflammation and tumorigenesis in APCmin/+ mice by releasing free Zn2+. In WT mice, a low dose of ZnO NPs (26 mg/kg/day) did not cause intestinal inflammation. In conclusion, higher doses and prolonged exposure to ZnO NPs promote the malignant transformation of precancerous epithelial cells.
ZnO nanoparticles promote the malignant transformation of colorectal epithelial cells in APCmin/+ mice
Meng, Jian (author) / Yang, Juan (author) / Pan, Ting (author) / Qu, Xianjun (author) / Cui, Shuxiang (author)
2021-10-05
Article (Journal)
Electronic Resource
English
| DOAJ | 2022
ZnO nanoparticles promote the malignant transformation of colorectal epithelial cells in APC mice
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