Analysis of metastasis suppressing function of E-cadherin in gastric cancer cells by RNAi

Zheng, Zhaohui; Sun, Xiuju; Zhou, Haitao; Shang, Chao; Ji, Hong; Sun, Kun

doi:10.3748/wjg.v11.i13.2000

Cited by 12 publications

(6 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…E-cadherin, a transmembrane protein expressed primarily in epithelial cells, mediates cellular adhesion necessary for formation of the junctional complex [18]. Reduced expression of E-cadherin has been regarded as one of the molecular events involved in invasion and metastasis of cancer cells [19]. We observed a significant correlation between loss of E-cadherin expression and lymph node metastases, suggesting cancer progression.…”

Section: Discussionmentioning

confidence: 55%

Gastric neuroendocrine carcinoma: Clinicopathologic review and immunohistochemical study of E‐cadherin and Ki‐67 as prognostic markers

Boo

Kim

Mok

et al. 2007

Journal of Surgical Oncology

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 55%

Gastric neuroendocrine carcinoma: Clinicopathologic review and immunohistochemical study of E‐cadherin and Ki‐67 as prognostic markers

Boo

Kim

Mok

et al. 2007

Journal of Surgical Oncology

View full text Add to dashboard Cite

show abstract

“…43 In this experiment, the mRNA level of CDH1 was completely silenced, and was accompanied by increased invasive capacity (1.5 fold). Other experiments have also been done to investigate whether the invasion suppressor function of CDH1 is mediated directly by tighter physical cell adhesion, indirectly by sequestering β-catenin and thus antagonizing β-catenin/ T-cell factor (TCF) signaling, or by other signaling pathways.…”

Section: E-cadherin (Cdh1)mentioning

confidence: 96%

Genomic and epigenetic profiles of gastric cancer: Potential diagnostic and therapeutic applications

2010

View full text Add to dashboard Cite

Knowledge about the molecular profile of tumor tissues is crucial to effectively target cancer cells, because cancer is a genetic disease that involves multiple genetic and epigenetic alterations. Prominent aberrations include gene mutation, amplification, loss or deletion, as well as epigenetic alterations of the promoter DNA CpG islands. All of these aberrations can lead to dynamic changes in cancer cells, as demonstrated using resected tumor samples. There are two distinct pathological types of gastric cancer: the diffuse type and the intestinal type of gastric cancer. Diffuse type gastric cancer harbors aberrations in the FGFR2/ErbB3/PI3 kinase pathway, while intestinal type gastric cancer has an activated ErbB2 oncogenic pathway. On the other hand, the prometastatic oncogene PRL-3 is commonly activated in both types of advanced gastric cancer, and might represent a relevant therapeutic target for gastric cancer with lymph node metastasis or peritoneal dissemination. Numerous tumor suppressor genes can inhibit such oncogenic pathways, and DNA methylation in CpG islands of gene promoters is frequently found to suppress the expression of such genes in gastric cancer. Helicobacter pylori infection in normal gastric mucosa may cause p53 mutations through activation of activation-induced cytidine deaminase (AID) and/or promoter DNA methylation of E-cadherin, an initiator of gastric cancer, and such abnormalities are found even in the precancerous stage of gastric carcinogenesis. In addition, it has been demonstrated that there are highly relevant methylation genes involved in cancer (HRMGs) that exhibit very frequent cancer-specific methylation in gastric cancer. Such genes are potential targets for cancer treatment, and might also serve as biomarkers of gastric cancer for either the diagnosis or for determining the prognosis or the response to treatment.

show abstract

“…Recognised as playing a key role in all cell migratory dynamics, cell-cell and cell-matrix adhesion are particularly important during cancer invasion (Behrens et al, 1989;Byers et al, 1995;Larebeke et al, 1992;Le et al, 1998;Umbas et al, 1992;Zheng et al, 2005). The past few decades have witnessed intensive in vivo and in vitro research efforts focused on exploring the impact of adhesion on the morphology and direction of migratory tumour cell patterns arising in cancer invasion (Friedl et al, 1995;Kolega, 1981;Pierce et al, 1978).…”

Section: Introductionmentioning

confidence: 99%

Mathematical modelling of cancer invasion: Implications of cell adhesion variability for tumour infiltrative growth patterns

Domschke

Trucu

Gerisch

et al. 2014

Journal of Theoretical Biology

131

144

View full text Add to dashboard Cite

Cancer invasion, recognised as one of the hallmarks of cancer, is a complex, multiscale phenomenon involving many inter-related genetic, biochemical, cellular and tissue processes at different spatial and temporal scales. Central to invasion is the ability of cancer cells to alter and degrade an extracellular matrix. Combined with abnormal excessive proliferation and migration which is enabled and enhanced by altered cell-cell and cell-matrix adhesion, the cancerous mass can invade the neighbouring tissue. Along with tumour-induced angiogenesis, invasion is a key component of metastatic spread, ultimately leading to the formation of secondary tumours in other parts of the host body. In this paper we explore the spatio-temporal dynamics of a model of cancer invasion, where cell-cell and cell-matrix adhesion is accounted for through non-local interaction terms in a system of partial integro-differential equations. The change of adhesion properties during cancer growth and development is investigated here through time-dependent adhesion characteristics within the cell population as well as those between the cells and the components of the extracellular matrix. Our computational simulation results demonstrate a range of heterogeneous dynamics which are qualitatively similar to the invasive growth patterns observed in a number of different types of cancer, such as tumour infiltrative growth patterns (INF).

show abstract

Analysis of metastasis suppressing function of E-cadherin in gastric cancer cells by RNAi

Abstract: siRNA targeted at non-coding and coding sequence of E-cadherin showed significant inhibition on mRNA and protein expression. Inhibited E-cadherin expression results in increased invasion ability of cancer cells.

Cited by 12 publications

References 20 publications

Gastric neuroendocrine carcinoma: Clinicopathologic review and immunohistochemical study of E‐cadherin and Ki‐67 as prognostic markers

Gastric neuroendocrine carcinoma: Clinicopathologic review and immunohistochemical study of E‐cadherin and Ki‐67 as prognostic markers

Genomic and epigenetic profiles of gastric cancer: Potential diagnostic and therapeutic applications

Mathematical modelling of cancer invasion: Implications of cell adhesion variability for tumour infiltrative growth patterns

Contact Info

Product

Resources

About