Expression of metastasis suppressor gene (KAI1/CD82) in oral squamous cell carcinoma and its clinico-pathological significance

Imai, Yutaka; Sasaki, Taro; Shinagawa, Yasuhiro; Akimoto, Kayoko; Fujibayashi, Takashi

doi:10.1016/s1368-8375(01)00120-8

Cited by 22 publications

(17 citation statements)

References 7 publications

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“…The other is that signal transduction elements for enhanced cell motility; ligand binding to the epidermal growth factor receptor induces a sequential downstream signaling in which actin-binding proteins, calcium, and protein kinase C serve to increase cell motility through adhesion and actin cytoskeleton alterations. In addition, it was reported that the immunohistochemical KAI1 staining was decreased in tumor tissues from oral and esophageal SCC patients [14][15][16]. In this study, KAI1 expression inversely correlated with that of KITENIN between normal adjacent mucosa and tumor tissues, but not between non-metastatic and metastatic lymph nodes.…”

Section: Discussionmentioning

confidence: 50%

“…This observation suggests that the expression level of KITENIN is much better molecular marker for both the malignant tumor and the metastatic lymph nodes of HNSCC patients than that of KAI1. Moreover, it was suggested that the KAI1 gene may not be a useful predictor of prognosis of oral SCC, although decreased KAI1 expression may be associated with increased invasive ability of oral SCC [15]. Overall, these preliminary clinical data from 17 HNSCC patients strongly suggest that KITENIN expression is involved in the progression of SCC.…”

Section: 1mentioning

confidence: 96%

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KITENIN increases invasion and migration of mouse squamous cancer cells and promotes pulmonary metastasis in a mouse squamous tumor model

et al. 2009

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a b s t r a c t KAI1 C-terminal interacting tetraspanin (KITENIN) is reported to promote metastasis in mouse colon cancer models. We investigated the role of KITENIN on the progression of squamous cell carcinoma (SCC). In a preliminary clinical study using resected tissues from head and neck SCC patients, KITE-NIN was highly expressed in tumors and metastatic lymph nodes, while KAI1 was more increased in adjacent mucosa than in tumor. KITENIN-transfected mouse squamous cancer (SCC VII/KITENIN) cells showed significantly higher invasion, migration, and proliferation than empty vector-transfected cells. In syngeneic mouse squamous tumor models, more increased tumor volume and enhanced lung metastasis were found in SCC VII/KITENIN cells-injected mice. Thus, KITENIN increases invasion and migration of squamous cancer cells and thereby promotes distant metastasis in mouse squamous tumor models.

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Section: Discussionmentioning

confidence: 50%

Section: 1mentioning

confidence: 96%

KITENIN increases invasion and migration of mouse squamous cancer cells and promotes pulmonary metastasis in a mouse squamous tumor model

et al. 2009

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“…The expression of KAI-1 has been seen to decrease in cancer cell lines with high propensity for metastasis. [9][10][11][12] Cancer cells expressing KAI-1 attach to vascular endothelial cells through direct interaction between KAI-1 and DAR (an endothelial cell surface protein), leading to inhibition of tumour cell proliferation and induction of positivity. Our results are in partial agreement with their study as KAI-1 expression in dentigerous and radicular cysts were nearly comparable with their studies although OKCs exhibited KAI-1 positivity to a lesser extent.…”

Section: Discussionmentioning

confidence: 99%

“…[7] Wu Q identified the role of KAI-1 in digestive tract carcinomas and predicted it to be a useful predictor of prognosis. [8] Farhadieh RD [9] and Imai Y [10] identified the role of KAI-1 in oral squamous cell carcinoma (OSCC) and suggested a decreased gene expression being associated with an increased invasive ability of OSCC. The expression of KAI-1/CD82 gene, inversely related to tumour progression, can, thus, be taken as a favourable prognostic indicator.…”

Section: Methodsmentioning

confidence: 99%

KAI-1 and p53 expression in odontogenic cysts: An immunohistochemical (IHC) marker study

Patil¹,

Wadhwan²,

Chowdhary³

et al. 2017

Oncobiology and Targets

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Background: KAI-1/CD82 is a tumour suppressor gene; decreased gene expression is associated with the increased invasive ability of oral squamous cell carcinoma (OSCC), as hypothesised for various odontogenic cysts and tumours. p53 protein functions in the G1-S phase of the cell cycle to allow repair of the damaged DNA. In the present study, p53 and KAI-1 expression was investigated by using monoclonal antibodies in the various odontogenic cysts. Aims: To detect KAI-1 and p53 expression in radicular cysts, dentigerous cysts and odontogenic keratocysts (OKCs) and to assess the relation between p53 and KAI-1 expression in the aforementioned cysts. Materials and Methods: The present study included histopathologically diagnosed cases of radicular cysts, dentigerous cysts and OKCs for the expression of KAI-1 and p53 antibodies. Results: Amongst odontogenic cysts, radicular cysts expressed a maximum positivity of KAI-1 (20.92%) while p53 positive cells were maximum in odontogenic keratocysts (4.04%). The correlation between KAI-1 and p53 expression in the various odontogenic cysts was not found to be significant. Conclusion: The increased KAI-1 expression in the radicular cysts and its downregulation in OKCs may be indicative of aggressive clinical behaviour and the fact that OKCs are hypothesised as neoplastic rather than being developmental in origin.

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“…In addition, oncogene activation, tumor suppressor gene inactivation (i.e. CD82), and the downregulation of cell-cell contact proteins, such as E-cadherin and β-catenin, were described in OSCC [32,54,78,92,96,113,182]. OSCC is derived from malignant keratinocytes and their corresponding malignant stem cells may be found in the stratum basale of the oral and dermal epithelium, which has been identified in immunohistochemical studies to harbor epithelial stem cells.…”

Section: Oral Squamous Cell Carcinomamentioning

confidence: 99%

Cancer stem cells as targets for cancer therapy: selected cancers as examples

Hombach‐Klonisch

Paranjothy

Wiecheć

et al. 2008

Arch. Immunol. Ther. Exp.

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It is becoming increasingly evident that cancer constitutes a group of diseases involving altered stem-cell maturation/differentiation and the disturbance of regenerative processes. The observed malignant transformation is merely a symptom of normal differentiation processes gone astray rather than the primary event. This review focuses on the role of cancer stem cells (CSCs) in three common but also relatively under-investigated cancers: head and neck, ovarian, and testicular cancer. For didactic purpose, the physiology of stem cells is first introduced using hematopoietic and mesenchymal stem cells as examples. This is followed by a discussion of the (possible) role of CSCs in head and neck, ovarian, and testicular cancer. Aside from basic information about the pathophysiology of these cancers, current research results focused on the discovery of molecular markers specific to these cancers are also discussed. The last part of the review is largely dedicated to signaling pathways active within various normal and CSC types (e.g. Nanog, Nestin, Notch1, Notch2, Oct3 and 4, Wnt). Different elements of these pathways are also discussed in the context

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Expression of metastasis suppressor gene (KAI1/CD82) in oral squamous cell carcinoma and its clinico-pathological significance

Cited by 22 publications

References 7 publications

KITENIN increases invasion and migration of mouse squamous cancer cells and promotes pulmonary metastasis in a mouse squamous tumor model

KITENIN increases invasion and migration of mouse squamous cancer cells and promotes pulmonary metastasis in a mouse squamous tumor model

KAI-1 and p53 expression in odontogenic cysts: An immunohistochemical (IHC) marker study

Cancer stem cells as targets for cancer therapy: selected cancers as examples

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