The clinical significance of vimentin-expressing gastric cancer cells in bone marrow

Masaaki Iwatsuki, Koshi Mimori, Takeo Fukagawa, Hideshi Ishii, Takehiko Yokobori, Mitsuru Sasako, Hideo Baba, Masaki Mori

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Background: Expression of the mesenchymal marker gene vimentin (VIM) in gastric cancer is associated with a more aggressive form of the disease and poor prognosis. Because epithelial mesenchymal transition (EMT) plays a critical role in the progression of gastric cancer, VIM expression was examined in the bone marrow (BM) of gastric cancer patients. Methods: BM samples from 437 gastric cancer patients were collected and analyzed by quantitative RT-PCR. Expression of VIM protein in the primary lesions of resected gastric cancers was evaluated using immunohistochemistry. Furthermore, induction of VIM expression by TGF-β1 and hypoxia was evaluated in gastric cancer cells. Results: VIM mRNA expression increased concordantly with clinical staging and was significantly associated with tumor invasion and lymph node metastasis (P < .0001). Though cancer cells in the primary lesions did not stain with VIM antibody, some of the cells invading the intratumoral vessels were strongly positive for VIM, but were negative for E-cadherin. Hypoxic conditions and treatment with TGF-β1 induced VIM expression and repressed E-cadherin in gastric cancer cells, coupled with an alteration of cellular morphology. Conclusions: We found that gastric cancer cells undergo EMT in BM to survive and metastasize. These findings suggest that isolated tumor cells have the potential to undergo EMT, which could increase the malignancy of gastric cancer.

Original languageEnglish
Pages (from-to)2526-2533
Number of pages8
JournalAnnals of Surgical Oncology
Volume17
Issue number9
DOIs
Publication statusPublished - Sep 1 2010

Fingerprint

Vimentin
Bone Marrow Cells
Stomach Neoplasms
Epithelial-Mesenchymal Transition
Bone Marrow
Cadherins
Neoplasms
Coloring Agents
Lymph Nodes
Immunohistochemistry
Neoplasm Metastasis
Polymerase Chain Reaction
Messenger RNA
Antibodies

All Science Journal Classification (ASJC) codes

  • Surgery
  • Oncology

Cite this

The clinical significance of vimentin-expressing gastric cancer cells in bone marrow. / Iwatsuki, Masaaki; Mimori, Koshi; Fukagawa, Takeo; Ishii, Hideshi; Yokobori, Takehiko; Sasako, Mitsuru; Baba, Hideo; Mori, Masaki.

In: Annals of Surgical Oncology, Vol. 17, No. 9, 01.09.2010, p. 2526-2533.

Research output: Contribution to journalArticle

Iwatsuki, Masaaki ; Mimori, Koshi ; Fukagawa, Takeo ; Ishii, Hideshi ; Yokobori, Takehiko ; Sasako, Mitsuru ; Baba, Hideo ; Mori, Masaki. / The clinical significance of vimentin-expressing gastric cancer cells in bone marrow. In: Annals of Surgical Oncology. 2010 ; Vol. 17, No. 9. pp. 2526-2533.
@article{8df3f9da6e1348efb70110bd3a0703e5,
title = "The clinical significance of vimentin-expressing gastric cancer cells in bone marrow",
abstract = "Background: Expression of the mesenchymal marker gene vimentin (VIM) in gastric cancer is associated with a more aggressive form of the disease and poor prognosis. Because epithelial mesenchymal transition (EMT) plays a critical role in the progression of gastric cancer, VIM expression was examined in the bone marrow (BM) of gastric cancer patients. Methods: BM samples from 437 gastric cancer patients were collected and analyzed by quantitative RT-PCR. Expression of VIM protein in the primary lesions of resected gastric cancers was evaluated using immunohistochemistry. Furthermore, induction of VIM expression by TGF-β1 and hypoxia was evaluated in gastric cancer cells. Results: VIM mRNA expression increased concordantly with clinical staging and was significantly associated with tumor invasion and lymph node metastasis (P < .0001). Though cancer cells in the primary lesions did not stain with VIM antibody, some of the cells invading the intratumoral vessels were strongly positive for VIM, but were negative for E-cadherin. Hypoxic conditions and treatment with TGF-β1 induced VIM expression and repressed E-cadherin in gastric cancer cells, coupled with an alteration of cellular morphology. Conclusions: We found that gastric cancer cells undergo EMT in BM to survive and metastasize. These findings suggest that isolated tumor cells have the potential to undergo EMT, which could increase the malignancy of gastric cancer.",
author = "Masaaki Iwatsuki and Koshi Mimori and Takeo Fukagawa and Hideshi Ishii and Takehiko Yokobori and Mitsuru Sasako and Hideo Baba and Masaki Mori",
year = "2010",
month = "9",
day = "1",
doi = "10.1245/s10434-010-1041-0",
language = "English",
volume = "17",
pages = "2526--2533",
journal = "Annals of Surgical Oncology",
issn = "1068-9265",
publisher = "Springer New York",
number = "9",

}

TY - JOUR

T1 - The clinical significance of vimentin-expressing gastric cancer cells in bone marrow

AU - Iwatsuki, Masaaki

AU - Mimori, Koshi

AU - Fukagawa, Takeo

AU - Ishii, Hideshi

AU - Yokobori, Takehiko

AU - Sasako, Mitsuru

AU - Baba, Hideo

AU - Mori, Masaki

PY - 2010/9/1

Y1 - 2010/9/1

N2 - Background: Expression of the mesenchymal marker gene vimentin (VIM) in gastric cancer is associated with a more aggressive form of the disease and poor prognosis. Because epithelial mesenchymal transition (EMT) plays a critical role in the progression of gastric cancer, VIM expression was examined in the bone marrow (BM) of gastric cancer patients. Methods: BM samples from 437 gastric cancer patients were collected and analyzed by quantitative RT-PCR. Expression of VIM protein in the primary lesions of resected gastric cancers was evaluated using immunohistochemistry. Furthermore, induction of VIM expression by TGF-β1 and hypoxia was evaluated in gastric cancer cells. Results: VIM mRNA expression increased concordantly with clinical staging and was significantly associated with tumor invasion and lymph node metastasis (P < .0001). Though cancer cells in the primary lesions did not stain with VIM antibody, some of the cells invading the intratumoral vessels were strongly positive for VIM, but were negative for E-cadherin. Hypoxic conditions and treatment with TGF-β1 induced VIM expression and repressed E-cadherin in gastric cancer cells, coupled with an alteration of cellular morphology. Conclusions: We found that gastric cancer cells undergo EMT in BM to survive and metastasize. These findings suggest that isolated tumor cells have the potential to undergo EMT, which could increase the malignancy of gastric cancer.

AB - Background: Expression of the mesenchymal marker gene vimentin (VIM) in gastric cancer is associated with a more aggressive form of the disease and poor prognosis. Because epithelial mesenchymal transition (EMT) plays a critical role in the progression of gastric cancer, VIM expression was examined in the bone marrow (BM) of gastric cancer patients. Methods: BM samples from 437 gastric cancer patients were collected and analyzed by quantitative RT-PCR. Expression of VIM protein in the primary lesions of resected gastric cancers was evaluated using immunohistochemistry. Furthermore, induction of VIM expression by TGF-β1 and hypoxia was evaluated in gastric cancer cells. Results: VIM mRNA expression increased concordantly with clinical staging and was significantly associated with tumor invasion and lymph node metastasis (P < .0001). Though cancer cells in the primary lesions did not stain with VIM antibody, some of the cells invading the intratumoral vessels were strongly positive for VIM, but were negative for E-cadherin. Hypoxic conditions and treatment with TGF-β1 induced VIM expression and repressed E-cadherin in gastric cancer cells, coupled with an alteration of cellular morphology. Conclusions: We found that gastric cancer cells undergo EMT in BM to survive and metastasize. These findings suggest that isolated tumor cells have the potential to undergo EMT, which could increase the malignancy of gastric cancer.

UR - http://www.scopus.com/inward/record.url?scp=77956343867&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77956343867&partnerID=8YFLogxK

U2 - 10.1245/s10434-010-1041-0

DO - 10.1245/s10434-010-1041-0

M3 - Article

C2 - 20358301

AN - SCOPUS:77956343867

VL - 17

SP - 2526

EP - 2533

JO - Annals of Surgical Oncology

JF - Annals of Surgical Oncology

SN - 1068-9265

IS - 9

ER -