Circadian disruption accelerates tumor growth and angio/stromagenesis through a wnt signaling pathway

Yoshihiro Yasuniwa, Hiroto Izumi, Ke Yong Wang, Shohei Shimajiri, Yasuyuki Sasaguri, Kazuaki Kawai, Hiroshi Kasai, Takashi Shimada, Koichi Miyake, Eiji Kashiwagi, Gen Hirano, Akihiko Kidani, Masaki Akiyama, Bin Han, Ying Wu, Ichiro Ieiri, Shun Higuchi, Kimitoshi Kohno

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Abstract

Epidemiologic studies show a high incidence of cancer in shift workers, suggesting a possible relationship between circadian rhythms and tumorigenesis. However, the precise molecular mechanism played by circadian rhythms in tumor progression is not known. To identify the possible mechanisms underlying tumor progression related to circadian rhythms, we set up nude mouse xenograft models. HeLa cells were injected in nude mice and nude mice were moved to two different cases, one case is exposed to a 24-hour light cycle (L/L), the other is a more ''normal'' 12-hour light/dark cycle (L/D). We found a significant increase in tumor volume in the L/L group compared with the L/D group. In addition, tumor microvessels and stroma were strongly increased in L/L mice. Although there was a hypervascularization in L/L tumors, there was no associated increase in the production of vascular endothelial cell growth factor (VEGF). DNA microarray analysis showed enhanced expression of WNT10A, and our subsequent study revealed that WNT10A stimulates the growth of both microvascular endothelial cells and fibroblasts in tumors from light-stressed mice, along with marked increases in angio/ stromagenesis. Only the tumor stroma stained positive for WNT10A and WNT10A is also highly expressed in keloid dermal fibroblasts but not in normal dermal fibroblasts indicated that WNT10A may be a novel angio/stromagenic growth factor. These findings suggest that circadian disruption induces the progression of malignant tumors via a Wnt signaling pathway. Copyright:

Original languageEnglish
Article numbere15330
JournalPloS one
Volume5
Issue number12
DOIs
Publication statusPublished - Dec 1 2010

Fingerprint

Wnt Signaling Pathway
Tumors
neoplasms
Growth
Neoplasms
Photoperiod
Fibroblasts
Circadian Rhythm
Nude Mice
circadian rhythm
fibroblasts
Endothelial cells
photoperiod
mice
Intercellular Signaling Peptides and Proteins
growth factors
endothelial cells
Keloid
Skin
Cell growth

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)
  • General

Cite this

Yasuniwa, Y., Izumi, H., Wang, K. Y., Shimajiri, S., Sasaguri, Y., Kawai, K., ... Kohno, K. (2010). Circadian disruption accelerates tumor growth and angio/stromagenesis through a wnt signaling pathway. PloS one, 5(12), [e15330]. https://doi.org/10.1371/journal.pone.0015330

Circadian disruption accelerates tumor growth and angio/stromagenesis through a wnt signaling pathway. / Yasuniwa, Yoshihiro; Izumi, Hiroto; Wang, Ke Yong; Shimajiri, Shohei; Sasaguri, Yasuyuki; Kawai, Kazuaki; Kasai, Hiroshi; Shimada, Takashi; Miyake, Koichi; Kashiwagi, Eiji; Hirano, Gen; Kidani, Akihiko; Akiyama, Masaki; Han, Bin; Wu, Ying; Ieiri, Ichiro; Higuchi, Shun; Kohno, Kimitoshi.

In: PloS one, Vol. 5, No. 12, e15330, 01.12.2010.

Research output: Contribution to journalArticle

Yasuniwa, Y, Izumi, H, Wang, KY, Shimajiri, S, Sasaguri, Y, Kawai, K, Kasai, H, Shimada, T, Miyake, K, Kashiwagi, E, Hirano, G, Kidani, A, Akiyama, M, Han, B, Wu, Y, Ieiri, I, Higuchi, S & Kohno, K 2010, 'Circadian disruption accelerates tumor growth and angio/stromagenesis through a wnt signaling pathway', PloS one, vol. 5, no. 12, e15330. https://doi.org/10.1371/journal.pone.0015330
Yasuniwa, Yoshihiro ; Izumi, Hiroto ; Wang, Ke Yong ; Shimajiri, Shohei ; Sasaguri, Yasuyuki ; Kawai, Kazuaki ; Kasai, Hiroshi ; Shimada, Takashi ; Miyake, Koichi ; Kashiwagi, Eiji ; Hirano, Gen ; Kidani, Akihiko ; Akiyama, Masaki ; Han, Bin ; Wu, Ying ; Ieiri, Ichiro ; Higuchi, Shun ; Kohno, Kimitoshi. / Circadian disruption accelerates tumor growth and angio/stromagenesis through a wnt signaling pathway. In: PloS one. 2010 ; Vol. 5, No. 12.
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