Autocrine galectin-1 promotes collective cell migration of squamous cell carcinoma cells through up-regulation of distinct integrins

Andra Rizqiawan; Kei Tobiume; Gaku Okui; Kazuhiro Yamamoto; Hideo Shigeishi; Shigehiro Ono; Hiroshi Shimasue; Masaaki Takechi; Koichiro Higashikawa; Nobuyuki Kamata

doi:10.1016/j.bbrc.2013.10.152

Autocrine galectin-1 promotes collective cell migration of squamous cell carcinoma cells through up-regulation of distinct integrins

Andra Rizqiawan, Kei Tobiume, Gaku Okui, Kazuhiro Yamamoto, Hideo Shigeishi, Shigehiro Ono, Hiroshi Shimasue, Masaaki Takechi, Koichiro Higashikawa, Nobuyuki Kamata

Research output: Contribution to journal › Article › peer-review

19 Citations (Scopus)

Abstract

We found that high galectin-1 (Gal-1) mRNA levels were associated with invasive squamous cell carcinoma (SCC) cells that expressed Snail, an epithelial-to-mesenchymal transition (EMT) regulator. Both Gal-1 overexpression and soluble Gal-1 treatment accelerated invasion and collective cell migration, along with activation of cdc42 and Rac. Soluble Gal-1 activated c-Jun N-terminal kinase to increase expression levels of integrins α2 and β5, which were essential for Gal-1 dependent collective cell migration and invasiveness. Soluble Gal-1 also increased the incidence of EMT in Snail-expressing SCC cells; these were a minor population with an EMT phenotype under growing conditions. Our findings indicate that soluble Gal-1 promotes invasiveness through enhancing collective cell migration and increasing the incidence of EMT.

Original language	English
Pages (from-to)	904-910
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	441
Issue number	4
DOIs	https://doi.org/10.1016/j.bbrc.2013.10.152
Publication status	Published - 29 Nov 2013
Externally published	Yes

Keywords

Collective cell migration
EMT
Galectin-1
Snail

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10.1016/j.bbrc.2013.10.152

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Rizqiawan, A., Tobiume, K., Okui, G., Yamamoto, K., Shigeishi, H., Ono, S., Shimasue, H., Takechi, M., Higashikawa, K., & Kamata, N. (2013). Autocrine galectin-1 promotes collective cell migration of squamous cell carcinoma cells through up-regulation of distinct integrins. Biochemical and Biophysical Research Communications, 441(4), 904-910. https://doi.org/10.1016/j.bbrc.2013.10.152

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title = "Autocrine galectin-1 promotes collective cell migration of squamous cell carcinoma cells through up-regulation of distinct integrins",

abstract = "We found that high galectin-1 (Gal-1) mRNA levels were associated with invasive squamous cell carcinoma (SCC) cells that expressed Snail, an epithelial-to-mesenchymal transition (EMT) regulator. Both Gal-1 overexpression and soluble Gal-1 treatment accelerated invasion and collective cell migration, along with activation of cdc42 and Rac. Soluble Gal-1 activated c-Jun N-terminal kinase to increase expression levels of integrins α2 and β5, which were essential for Gal-1 dependent collective cell migration and invasiveness. Soluble Gal-1 also increased the incidence of EMT in Snail-expressing SCC cells; these were a minor population with an EMT phenotype under growing conditions. Our findings indicate that soluble Gal-1 promotes invasiveness through enhancing collective cell migration and increasing the incidence of EMT.",

keywords = "Collective cell migration, EMT, Galectin-1, Snail",

author = "Andra Rizqiawan and Kei Tobiume and Gaku Okui and Kazuhiro Yamamoto and Hideo Shigeishi and Shigehiro Ono and Hiroshi Shimasue and Masaaki Takechi and Koichiro Higashikawa and Nobuyuki Kamata",

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Rizqiawan, A, Tobiume, K, Okui, G, Yamamoto, K, Shigeishi, H, Ono, S, Shimasue, H, Takechi, M, Higashikawa, K & Kamata, N 2013, 'Autocrine galectin-1 promotes collective cell migration of squamous cell carcinoma cells through up-regulation of distinct integrins', Biochemical and Biophysical Research Communications, vol. 441, no. 4, pp. 904-910. https://doi.org/10.1016/j.bbrc.2013.10.152

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T1 - Autocrine galectin-1 promotes collective cell migration of squamous cell carcinoma cells through up-regulation of distinct integrins

AU - Rizqiawan, Andra

AU - Tobiume, Kei

AU - Okui, Gaku

AU - Yamamoto, Kazuhiro

AU - Shigeishi, Hideo

AU - Ono, Shigehiro

AU - Shimasue, Hiroshi

AU - Takechi, Masaaki

AU - Higashikawa, Koichiro

AU - Kamata, Nobuyuki

PY - 2013/11/29

Y1 - 2013/11/29

N2 - We found that high galectin-1 (Gal-1) mRNA levels were associated with invasive squamous cell carcinoma (SCC) cells that expressed Snail, an epithelial-to-mesenchymal transition (EMT) regulator. Both Gal-1 overexpression and soluble Gal-1 treatment accelerated invasion and collective cell migration, along with activation of cdc42 and Rac. Soluble Gal-1 activated c-Jun N-terminal kinase to increase expression levels of integrins α2 and β5, which were essential for Gal-1 dependent collective cell migration and invasiveness. Soluble Gal-1 also increased the incidence of EMT in Snail-expressing SCC cells; these were a minor population with an EMT phenotype under growing conditions. Our findings indicate that soluble Gal-1 promotes invasiveness through enhancing collective cell migration and increasing the incidence of EMT.

AB - We found that high galectin-1 (Gal-1) mRNA levels were associated with invasive squamous cell carcinoma (SCC) cells that expressed Snail, an epithelial-to-mesenchymal transition (EMT) regulator. Both Gal-1 overexpression and soluble Gal-1 treatment accelerated invasion and collective cell migration, along with activation of cdc42 and Rac. Soluble Gal-1 activated c-Jun N-terminal kinase to increase expression levels of integrins α2 and β5, which were essential for Gal-1 dependent collective cell migration and invasiveness. Soluble Gal-1 also increased the incidence of EMT in Snail-expressing SCC cells; these were a minor population with an EMT phenotype under growing conditions. Our findings indicate that soluble Gal-1 promotes invasiveness through enhancing collective cell migration and increasing the incidence of EMT.

KW - Collective cell migration

KW - EMT

KW - Galectin-1

KW - Snail

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ER -

Autocrine galectin-1 promotes collective cell migration of squamous cell carcinoma cells through up-regulation of distinct integrins

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Keywords

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