Recombinant Erdr1 suppresses the migration and invasion ability of human gastric cancer cells, SNU-216, through the JNK pathway

Min Kyung Jung, Youn Kyung Houh, Soogyeong Ha, Yoolhee Yang, Daejin Kim, Tae Sung Kim, Suk Ran Yoon, Sa Ik Bang, Byung Joo Cho, Wang Jae Lee, Hyunjeong Park, Dae Ho Cho

Research output: Contribution to journalArticle

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Abstract

Erythroid differentiation regulator 1 (Erdr1) suppressed cell motility in vitro and has anti-metastatic effect in vivo on melanoma. The current study investigated the effect of recombinant Erdr1 on the migration and invasion ability of SNU-216 cell, a gastric cancer cell line. The expression of Erdr1 is inversely correlated with IL-18 expression, which has a pro-cancer effect in gastric cancer. Treatment with rErdr1 markedly suppressed the ability of SNU-216 cells to migrate and invade, indicating that recombinant Erdr1 inhibited the motility of gastric cancer cells. E-cadherin expression levels were measured to determine the factor involved in the rErdr1-suppressed motility. E-cadherin is a representative of the cadherin family, known as cell motility enhancement adhesion molecule. Our results revealed that E-cadherin levels were increased by rErdr1 treatment, suggesting the involvement of E-cadherin in rErdr1-reduced cell migration. The cells were treated with specific MAPK inhibitors such as SP600125, SB203580 or PD98059 to identify the signaling mechanism involved with rErdr1 suppressed cell migration. The results indicated that the rErdr1 inhibited migration was primarily reversed by SP600125, a JNK inhibitor. In addition, the level of JNK phosphorylation was markedly increased by recombinant Erdr1. Taken together, these findings suggest that rErdr1 suppressed the ability of gastric cancer cells to metastasis by up regulating E-cadherin through a JNK pathway activation. Furthermore, it can be suggested that the inhibitory effect of recombinant Erdr1 on SNU-216 cell's metastatic potential was through cell motility suppression.

Original languageEnglish
Pages (from-to)145-151
Number of pages7
JournalImmunology Letters
Volume150
Issue number1-2
DOIs
Publication statusPublished - 2013 Feb 1

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MAP Kinase Signaling System
Cadherins
Stomach Neoplasms
Cell Movement
Interleukin-18
Melanoma
Phosphorylation
Neoplasm Metastasis
Cell Line
Neoplasms

Keywords

  • E-cadherin
  • Erdr1
  • Erythroid differentiation regulator 1
  • Gastric cancer
  • Invasion
  • JNK
  • Migration

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Recombinant Erdr1 suppresses the migration and invasion ability of human gastric cancer cells, SNU-216, through the JNK pathway. / Jung, Min Kyung; Houh, Youn Kyung; Ha, Soogyeong; Yang, Yoolhee; Kim, Daejin; Kim, Tae Sung; Yoon, Suk Ran; Bang, Sa Ik; Cho, Byung Joo; Lee, Wang Jae; Park, Hyunjeong; Cho, Dae Ho.

In: Immunology Letters, Vol. 150, No. 1-2, 01.02.2013, p. 145-151.

Research output: Contribution to journalArticle

Jung, Min Kyung ; Houh, Youn Kyung ; Ha, Soogyeong ; Yang, Yoolhee ; Kim, Daejin ; Kim, Tae Sung ; Yoon, Suk Ran ; Bang, Sa Ik ; Cho, Byung Joo ; Lee, Wang Jae ; Park, Hyunjeong ; Cho, Dae Ho. / Recombinant Erdr1 suppresses the migration and invasion ability of human gastric cancer cells, SNU-216, through the JNK pathway. In: Immunology Letters. 2013 ; Vol. 150, No. 1-2. pp. 145-151.
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abstract = "Erythroid differentiation regulator 1 (Erdr1) suppressed cell motility in vitro and has anti-metastatic effect in vivo on melanoma. The current study investigated the effect of recombinant Erdr1 on the migration and invasion ability of SNU-216 cell, a gastric cancer cell line. The expression of Erdr1 is inversely correlated with IL-18 expression, which has a pro-cancer effect in gastric cancer. Treatment with rErdr1 markedly suppressed the ability of SNU-216 cells to migrate and invade, indicating that recombinant Erdr1 inhibited the motility of gastric cancer cells. E-cadherin expression levels were measured to determine the factor involved in the rErdr1-suppressed motility. E-cadherin is a representative of the cadherin family, known as cell motility enhancement adhesion molecule. Our results revealed that E-cadherin levels were increased by rErdr1 treatment, suggesting the involvement of E-cadherin in rErdr1-reduced cell migration. The cells were treated with specific MAPK inhibitors such as SP600125, SB203580 or PD98059 to identify the signaling mechanism involved with rErdr1 suppressed cell migration. The results indicated that the rErdr1 inhibited migration was primarily reversed by SP600125, a JNK inhibitor. In addition, the level of JNK phosphorylation was markedly increased by recombinant Erdr1. Taken together, these findings suggest that rErdr1 suppressed the ability of gastric cancer cells to metastasis by up regulating E-cadherin through a JNK pathway activation. Furthermore, it can be suggested that the inhibitory effect of recombinant Erdr1 on SNU-216 cell's metastatic potential was through cell motility suppression.",
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AU - Jung, Min Kyung

AU - Houh, Youn Kyung

AU - Ha, Soogyeong

AU - Yang, Yoolhee

AU - Kim, Daejin

AU - Kim, Tae Sung

AU - Yoon, Suk Ran

AU - Bang, Sa Ik

AU - Cho, Byung Joo

AU - Lee, Wang Jae

AU - Park, Hyunjeong

AU - Cho, Dae Ho

PY - 2013/2/1

Y1 - 2013/2/1

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AB - Erythroid differentiation regulator 1 (Erdr1) suppressed cell motility in vitro and has anti-metastatic effect in vivo on melanoma. The current study investigated the effect of recombinant Erdr1 on the migration and invasion ability of SNU-216 cell, a gastric cancer cell line. The expression of Erdr1 is inversely correlated with IL-18 expression, which has a pro-cancer effect in gastric cancer. Treatment with rErdr1 markedly suppressed the ability of SNU-216 cells to migrate and invade, indicating that recombinant Erdr1 inhibited the motility of gastric cancer cells. E-cadherin expression levels were measured to determine the factor involved in the rErdr1-suppressed motility. E-cadherin is a representative of the cadherin family, known as cell motility enhancement adhesion molecule. Our results revealed that E-cadherin levels were increased by rErdr1 treatment, suggesting the involvement of E-cadherin in rErdr1-reduced cell migration. The cells were treated with specific MAPK inhibitors such as SP600125, SB203580 or PD98059 to identify the signaling mechanism involved with rErdr1 suppressed cell migration. The results indicated that the rErdr1 inhibited migration was primarily reversed by SP600125, a JNK inhibitor. In addition, the level of JNK phosphorylation was markedly increased by recombinant Erdr1. Taken together, these findings suggest that rErdr1 suppressed the ability of gastric cancer cells to metastasis by up regulating E-cadherin through a JNK pathway activation. Furthermore, it can be suggested that the inhibitory effect of recombinant Erdr1 on SNU-216 cell's metastatic potential was through cell motility suppression.

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KW - Invasion

KW - JNK

KW - Migration

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