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Effects of Salivary Mg on Head and Neck Carcinoma via TRPM7

  • W. Qiao
    ,
  • X. M. Lan
    ,
  • H. X. Ma
    ,
  • J. Y.K. Chan
    ,
  • ,
  • K. W.K. Yeung
*Corresponding author for this work
  • The University of Hong Kong
    ,
  • Nanjing Medical University
    ,
  • Chinese University of Hong Kong
Scholary Output:
Contribution to journal
Article
Peer-review

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

Magnesium (Mg) has been known to play vital roles in regulating growth and various metabolic processes. In recent years, the association between Mg and tumorigenesis has raised more and more attention. However, the effects of Mg on the progression of head and neck carcinoma (HNC), as well as the mechanism behind it, remain undefined. In this study, the roles of Mg in tumorigenic activities were tested in CAL27 and FaDu cells as well as in a xenograft tumor model in nude mice. We demonstrated that a moderate increase in extracellular Mg contributed to the proliferation, migration, and invasion of 2 HNC cell lines, while the addition of Mg in drinking water promoted the growth of xenograft tumors in mice without altering their serum Mg levels. Moreover, TRPM7, a major Mg transporter, was shown to be essential for the tumorigenic activities of HNC and the Mg-induced promotive effects on HNC cells and was further shown to be associated with the activation of AKT/mTOR (mammalian target of rapamycin) signaling. In a preliminary clinical study, we determined the Mg ion concentrations in the stimulated saliva from 72 patients with nasopharynx carcinoma and 12 healthy individuals. Our data revealed that the salivary Mg levels of subjects with nasopharynx carcinoma were significantly higher than those of the healthy controls. This is correlated with our finding showing TRPM7 to be overexpressed in tumor tissues harvested from 9 patients with HNC. Therefore, we can conclude that salivary Mg level, within a certain range, could act as a risk factor for the progression of HNC, which involves the activation of AKT/mTOR signaling pathways through the TRPM7 channel. The control of salivary Mg level and the intervention of TRPM7 should not be ignored during the study of HNC.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 304-312 (9 pages)

Journal (Volume, Issue Number)

Journal of Dental Research (Volume 98, Issue 3)

Publication milestones

  • Published - 03/01/2019

Publication status

Published - 03/01/2019

ISSN

0022-0345

Publication IDs

  • Scopus: 85060519948
  • PubMed: 30513244

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Scopus
citations
Fractional count
1
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0.09
Fractional count
10
Fractional count
0.91
Fractional count
1
Fractional count
1

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Funding Details

We are grateful for the technical support from Chui Ying Yip, Ng Kim Hei, and Edith Tong in the University of Hong Kong. V.W.Y. Lui is funded by the Research Grant Council, Hong Kong (17114814, 17121616, General Research Fund; T12-401/13-R, Theme-Based Research Scheme). The project was supported by the Hong Kong Research Grant Council (17120718, General Research Fund), the University of Hong Kong’s Strategic Research Theme of Cancer Seed Fund for Collaboration (T12-401/13-R), and Shenzhen Science and Technology Funding (JCYJ20160429190821781, JCYJ20160429 185449249). V.W.Y. Lui is funded by the Research Grant Council, Hong Kong (17114814, 17121616, General Research Fund; T12-401/13-R, Theme-Based Research Scheme). Part of this study was presented at the 96th General Session of the International Association for Dental Research and received the LION Dental Research Award. We are grateful for the technical support from Chui Ying Yip, Ng Kim Hei, and Edith Tong in the University of Hong Kong. The authors declare no potential conflicts of interest with respect to the authorship and/or publication of this article.
FundersFunding numbers
Edith Tong in the University of Hong Kong
-
General Research Fund
-
Hong Kong Research Grant Council
17120718
Research Grant Council, Hong Kong
17121616, 17114814
Shenzhen Science and Technology Funding
JCYJ20160429 185449249, JCYJ20160429190821781
HKU
T12-401/13-R