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Journal of Zhejiang University SCIENCE B 1998 Vol.-1 No.-1 P.

http://doi.org/10.1631/jzus.B2300896


Chronic exposure to hexavalent chromium induces esophageal tumorigenesis via activating the Notch signaling pathway


Author(s):  Yilin ZHU, Fanrong LIU, Lei LIU, Jinfu WANG, Fengyuan GAO, Lan YE, Honglei WU, Chengjun ZHOU, Guimei LIN, Xiaogang ZHAO, Peichao LI

Affiliation(s):  Department of Thoracic Surgery, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, China; more

Corresponding email(s):   lipeichao@email.sdu.edu.cn

Key Words:  Hexavalent chromium [Cr(VI)], esophageal tumorigenesis, malignant proliferation, stemness, Notch signaling pathway


Yilin ZHU, Fanrong LIU, Lei LIU, Jinfu WANG, Fengyuan GAO, Lan YE, Honglei WU, Chengjun ZHOU, Guimei LIN, Xiaogang ZHAO, Peichao LI. Chronic exposure to hexavalent chromium induces esophageal tumorigenesis via activating the Notch signaling pathway[J]. Journal of Zhejiang University Science B, 1998, -1(-1): .

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%A Lan YE
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A1 - Lan YE
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A1 - Chengjun ZHOU
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DOI - 10.1631/jzus.B2300896


Abstract: 
hexavalent chromium [Cr(VI)], as a well-established carcinogen, contributes to tumorigenesis for many human cancers, especially respiratory and digestive tumors. However, the potential function and relevant mechanism of Cr(VI) on the initiation of esophageal carcinogenesis is largely unknown. Here, immortalized human esophageal epithelial cells (HEECs) were induced to be malignantly transformed cells, termed HEEC-Cr(VI) cells, via chronic exposure to Cr(VI), which simulates the progress of esophageal tumorigenesis. In vitro and in vivo experiments demonstrated that HEEC-Cr(VI) cells obtain the ability of anchorage-independent growth, greater proliferative capacity, cancer stem cell properties, and capacity to form subcutaneous xenografts in BALB/c nude mice when compared to its parental cells, HEECs. Additionally, HEEC-Cr(VI) cells exhibited weakened cell motility and enhanced cell adhesion. Interestingly, HEECs with acute exposure to Cr(VI) failed to display those malignant phenotypes of HEEC-Cr(VI) cells, suggesting that Cr(VI)-induced malignant transformation, but not Cr(VI) itself, is the cause for the tumor characteristics of HEEC-Cr(VI) cells. Mechanistically, chronic exposure to Cr(VI) induced abnormal activation of Notch signaling, which is crucial to maintaining the capacity for malignant proliferation and stemness of HEEC-Cr(VI) cells. As expected, DAPT, an inhibitor for the Notch pathway, drastically attenuated cancerous phenotypes of HEEC-Cr(VI) cells. In conclusion, our study clarified the molecular mechanism underlying Cr(VI)-induced esophageal tumorigenesis, which provides novel insights for further basic research and clinical therapeutic strategies about Cr(VI)-associated esophageal cancer.

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