Expression of Intercellular Adhesion Molecule-1 and E-Selectin in Gastric Cancer and Their Clinical Significance

Jung, Won Young; Jang, Young-Joo; Kim, Jong Han; Park, Seong Heum; Kim, Seungjoo; Mok, Young Jae; Kim, Chong Suk

doi:10.5230/jgc.2012.12.3.140

Cited by 33 publications

(31 citation statements)

References 27 publications

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“…Yashiro et al (60) suggested that ICAM-1 facilitates GC cell adhesion to immune cells, leading to immune tolerance (Table II). However, other studies have demonstrated an association between the serum levels of circulating ICAM-1 and GC tumor progression, with higher levels indicating a worse prognosis (53,61,62). On account of the contradictory results in these studies, ICAM-1 has not yet been established as a prognostic marker in GC.…”

Section: Lymphangiogenesis and Metastasismentioning

confidence: 67%

Molecular background of the regional lymph node metastasis of gastric cancer (Review)

Zhu

Hu²,

Wei

et al. 2018

Oncol Lett

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Abstract. Gastric cancer (GC) is one of the deadliest types of cancer in the world. Lymph node (LN) metastasis is a complex and malignant behavior of GC, involving a sequence of biological processes, including decreased adherence to adjacent cells, extracellular matrix (ECM) degradation and lymphatic channel permeation. LN metastasis is directly associated with the treatment response, local recurrence and long-term survival of patients with GC. Therefore, the molecular mechanisms of LN metastasis in GC development require further investigation. Recently, a large number of clinical studies have focused on the molecular mechanisms and biological markers of tumor invasion and metastasis. However, few articles have broadly summarized LN metastasis in GC, and the molecular mechanisms of LN metastasis are not yet fully understood. In the present review, the molecular mechanisms of LN metastasis in GC will be discussed, including the following aspects: Cell adhesion and movement, ECM degradation, new vessel formation, and molecular pattern differences between metastatic LNs and the primary tumor. This review may lead to a better understanding of LN metastasis in GC, and the identification of new diagnostic markers.

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Section: Lymphangiogenesis and Metastasismentioning

confidence: 67%

Molecular background of the regional lymph node metastasis of gastric cancer (Review)

Zhu

Hu²,

Wei

et al. 2018

Oncol Lett

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“…TIMP-1 from TIMPs has a strong affinity with MMP-9, and plays a direct or indirect inhibition role in other members from MMPs family [28]. ICAM-1, a glycoprotein, can promote migration and invasion of tumor cells, and plays an important role in tumor invasion and migration [29,30]. Our findings showed that after ZNF139 expression, expressions of MMP-2, MMP-9 and ICAM-1 were decreased, while TIMP-1 expression was increased, suggesting that ZNF139 gene was closely related to invasion and metastasis of gastric cancer and its regulatory mechanism might be caused by adjusting MMP-TIMP balance and ICAM-1.…”

Section: Discussionmentioning

confidence: 99%

ZNF139 promotes tumor metastasis by increasing migration and invasion in human gastric cancer cells

Li¹,

Tan²,

Zhao³

et al. 2014

neo

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Zinc finger protein 139(ZNF139), a member of zinc finger protein family, is a transcription factor. Our previous research showed ZNF139 was overexpressed in gastric cancer cells. The purpose of present study is to explore impact and mechanism of ZNF139 on metastasis by regulating invasive ability of gastric cancer cells.Quantitative RT-PCR(QRT-PCR) and Western blot were applied for detection of ZNF139 expression in gastric cancer tissues, adjacent cancer tissues, metastatic lymph nodes, gastric cancer cell lines SGC7901 and BGC823 and gastric epithelial cell line GES-1; siRNA specific to ZNF139 was synthesized and then transfected into gastric cancer cell line BGC823; wound healing assay and Transwell assay were used to observe impact of ZNF139-siRNA after being transfected into BGC823 on its invasion and migration; changes in expression of invasion and migration-related genes MMP-2, MMP-9, ICAM-1 and TIMP1 were detected before and after transfection. Gelatin zymogrphy assay were applied to determine the MMP activities. Statistical analysis was based on the SPSS11.5 software.Expression of ZNF139 in gastric adenocarcinoma tissues and cells was significantly higher than the expression in the adjacent cancer tissues, but lower than the expression in the metastatic lymph nodes; ZNF139 expression was present in gastric cancer cell lines, and the expression level was higher than that in normal gastric epithelial cells lines. ZNF139-siRNA significantly inhibited the invasion and migration activity of gastric cancer cell line BGC823. 48h after ZNF139-siRNA was transfected into gastric cancer cell line BGC823, expression and activity of invasion-related genes MMP-2, MMP-9, ICAM-1 mRNA and protein were significantly inhibited, while expressions of TIMP-1 mRNA and protein were significantly increased. At the same time, the gelatinase activities of MMP2 and MMP9 were decreased by ZNF139 interference.ZNF139 was overexpressed in gastric cancer cells, and the expression was further enhanced in the metastasis process. Knocking down ZNF139 expression in gastric cancer cells could effectively reduce gastric cancer cell invasion and migration ability, and this process might play a role by regulating MMP-TIMP balance. Key words: gastric cancer, zinc finger protein 139(ZNF139), migration, invasion, RNA interference technologyGastric cancer is currently the second leading cancer killer in the world. High incidence of gastric cancer exists in east Asia, which is also the leading cause of death in malignant tumor in China. Gastric cancer has strong ability for proliferation, invasion and metastasis, which is one of the important factors that lead to poor prognosis. A variety of genes in tumor cells and their expression products play an important role in the invasion and metastasis process of gastric cancer [1][2][3][4]. It has been a hotspot to treat gastric cancer by inhibiting invasion and migration capability of gastric cancer cells, and the study has made some achievements [5][6][7]. But there has yet not been a breakthrough in the...

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“…21 Increased expression of ICAM-1 may play an important role in the development of malignant tumours. [23][24][25] Although hypothyroidism has been reported to be responsible for an increased risk of atherosclerotic heart disease, outcomes of prospective studies are inconclusive. 26,27 One study revealed an association between SHO and atherosclerosis and myocardial infarction in older women, 26 and further studies have claimed that levothyroxine replacement therapy in those with manifest or SHO has improved atherosclerotic signs and symptoms.…”

Section: Discussionmentioning

confidence: 99%

“…34 The correlation between soluble forms of adhesion molecules and tumour-node-metastasis staging, and also between development of metastasis in gastric, colorectal and breast cancers has also been demonstrated. 24,33,35 The aim of the present study was to determine the correlation between TSH levels and sICAM-1, sVCAM-1 and E-selectin values in patients with SHO. In patients with SHO, pretreatment sICAM-1 levels were found to be significantly higher than those found in healthy controls (P ¼ 0.0001).…”

Section: Discussionmentioning

confidence: 99%

Subclinical hypothyroidism: Comparison of adhesion molecule levels before and after levothyroxine therapy

Bilgir

Çalan

et al. 2014

J Int Med Res

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Objective: Adhesion molecules are involved in inflammation, atherosclerosis and malignancy. This study measured levels of adhesion molecules before and after levothyroxine therapy in patients with subclinical hypothyroidism (SHO). Methods: Levels of soluble (s) intracellular adhesion molecule (ICAM)-1, s vascular cell adhesion molecule (sVCAM) VCAM-1 and sE-selectin were analysed in patients diagnosed with SHO, prior to administration of 50 mg/day levothyroxine orally for 3 months. Subsequently, levels of sICAM-1, sVCAM-1 and sE-selectin were reanalysed then compared with the pretreatment levels. Results: In 30 patients with SHO, levels of sICAM-1 were found to be significantly higher than those in healthy controls, (P ¼ 0.001). Post-treatment sICAM-1 levels were significantly lower than pretreatment levels (P ¼ 0.001). No significant differences were found in sVCAM-1 or sE-selectin levels between healthy controls and patients with SHO before treatment, or between patients with SHO pre-and post-treatment. Conclusions: Patients with SHO had significantly higher levels of sICAM-1 compared with controls. Levels became normal after treatment with levothyroxine. These findings emphasize the need for levothyroxine therapy in cases of SHO to normalize sICAM-1 levels. Such treatment helps to prevent the future development of atherosclerosis or cancer.

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Expression of Intercellular Adhesion Molecule-1 and E-Selectin in Gastric Cancer and Their Clinical Significance

Cited by 33 publications

References 27 publications

Molecular background of the regional lymph node metastasis of gastric cancer (Review)

Molecular background of the regional lymph node metastasis of gastric cancer (Review)

ZNF139 promotes tumor metastasis by increasing migration and invasion in human gastric cancer cells

Subclinical hypothyroidism: Comparison of adhesion molecule levels before and after levothyroxine therapy

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