KAI1/CD82 suppresses tumor invasion by MMP9 inactivation via TIMP1 up-regulation in the H1299 human lung carcinoma cell line

Jee, Bo Keun; Park, Koung Min; Surendran, Sibin; Lee, Woon Kyu; Han, Chang Whan; Kim, Yong Sik; Lim, Yejee

doi:10.1016/j.bbrc.2006.01.153

Cited by 56 publications

(47 citation statements)

References 21 publications

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“…33 Another report suggested that KAI1/CD82 accelerated the desensitization of EGF (epidermal growth factor) signaling and endocytosis of EGFR (epidermal growth factor receptor). 34 In previous reports, we suggested that KAI1/CD82 suppressed tumor-invasion by MMP9 inactivation via TIMP1 up-regulation 21 and cell migration through the inhibition of b1 integrin maturation in the H1299 human lung carcinoma cell line. 22 Cell migration, an essential process in tumor cell metastasis, is regulated by many extracellular cues including growth factors, cytokines and the extracellular matrix.…”

Section: Discussionmentioning

confidence: 89%

“…KAI1/CD82-transfectants were generated as described by Jee et al 21,22 Briefly, these cells were cultured in RPMI-1640 medium that contained 10% fetal bovine serum (FBS; Gibco, Grand Island, NY), penicillin (10 units/ml; Sigma, St. Louis, MO) and streptomycin (0.1 ml; Sigma). The pcDNA3.1-CD82 plasmid construct was stably transfected into H1299 cells (nonsmall cell lung carcinoma) using Lipofectamine (Invitrogen, Carlsbad, CA).…”

Section: Cell Culture and Transfectionmentioning

confidence: 99%

“…21 Briefly, three groups of H1299 cells (one study group and two control groups), each of which contained an equal number of cells (3 Â 10 5 cells per 100-mm culture dish at 60% confluency), were left untreated in SFM for 24 h at 378C in 5% CO 2 . The cells were then lysed and subjected to SDS-PAGE (sodium dodecyl sulfatepolyacrylamide gel electrophoresis) and Western blot analysis to detect levels of Ras (Calbiochem, Darmstadt, Germany), cdc42, Rho, PI3K, Akt (BD Transduction Laboratories, Los Angeles, CA), mTOR, p-mTOR (Cell Signaling Technology, Inc., Beverly, MA), Rac1 and CD82 (Santa Cruz Biotechnology, Santa Cruz, CA).…”

Section: Immunoblotting Analysismentioning

confidence: 99%

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KAI1/CD82 decreases Rac1 expression and cell proliferation through PI3K/Akt/mTOR pathway in H1299 lung carcinoma cells

Choi

Jee

Lim

et al. 2008

Cell Biochemistry & Function

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Although the KAI1/CD82 protein has been reported to inhibit cell metastasis in many studies, its mechanism of action has not yet been fully elucidated. In the present study, we investigated the possible effects of KAI1/CD82 on the metastatic phenotype in H1299 lung carcinoma cells. These studies were based on the pivotal role that the acquisition of motile phenotype plays on the initial steps of metastasis. KAI1/CD82-mediated morphological changes were observed using phase contrast microscopy. We report here, that a KAI1/CD82-induced phenotypic change was involved in the decrease of Rac1 expression and GTPase activity. However, we found that KAI1/CD82 did not regulate Rac1 mRNA levels. This suggests the existence of another regulatory mechanism of Rac1 protein maturation or activation. To identify the signaling pathway of Rac1 regulation, we investigated the PI3K/Akt/mTOR pathway, since the PI3K/Akt pathway regulates Rac1 activation and mTOR is known to play a regulatory role in protein translation. H1299/CD82-transfectants showed lower mTOR expression and cell growth than the control group. The data obtained from this study suggested that KAI1/CD82 decreased the metastatic phenotype of H1299 lung carcinoma cells by down-regulating Rac1 expression through the PI3K/Akt/mTOR pathway.

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Section: Discussionmentioning

confidence: 89%

Section: Cell Culture and Transfectionmentioning

confidence: 99%

Section: Immunoblotting Analysismentioning

confidence: 99%

See 1 more Smart Citation

KAI1/CD82 decreases Rac1 expression and cell proliferation through PI3K/Akt/mTOR pathway in H1299 lung carcinoma cells

Choi

Jee

Lim

et al. 2008

Cell Biochemistry & Function

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“…In fact, KAI1 lacks intrinsic activity, but mediates its functions via binding to surface receptors such as integrins or receptor tyrosine kinases in a cell specific manner [24]. Several attractive scenarios have been put forward to explain KAI1 anti-invasive effects; including upregulation of TIMP-1 [37] and the inactivation of urokinase receptor proteolytic activities [38]. Although previous studies have shown that several pro-and anti-metastatic factors are modulated by genistein treatment, these were done at supraphysiological levels and therefore might not recapitulate what is happening with the doses used in this study or what could be achieved via genistein consumption.…”

Section: Discussionmentioning

confidence: 99%

Genistein induces the metastasis suppressor kangai-1 which mediates its anti-invasive effects in TRAMP cancer cells

Touny¹,

Banerjee²

2007

Biochemical and Biophysical Research Communications

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Previous studies demonstrated a direct correlation with loss of kangai-1 (KAI1), a metastasis suppressor, and poor prognosis in human prostate and other cancers. In this study, we have characterized the age-dependent downregulation of KAI1 in the TRAMP model which was reversed when mice were fed a genistein-enriched diet. We demonstrated here that doses of genistein (5 and 10 μM) -which could be achieved by supplement intake-significantly induced the expression of KAI1, both at the mRNA and protein levels (up to 2.5-fold), and decreased the invasiveness of TRAMP-C2 cells by more than 2.0-fold. We have pinpointed KAI1 as the suppressor of invasion, since its targeted knockdown by siRNA restored the invasive potential of genistein-treated TRAMP-C2 cells to control levels. This work provides the first evidence that genistein treatment may counteract KAI1 downregulation, which is observed in many cancer types and therefore, could be used in anti-metastatic therapies.

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“…RT-PCR analysis was performed as described by Jee et al (2006). After the induction of osteogenic differentiation for 21 days, total RNA was isolated from the cells using an RNeasy Mini Kit (QIAGEN, Valencia, CA).…”

Section: Rna Isolation and Reverse Transcriptase-polymerase Chain Reamentioning

confidence: 99%

HOX gene analysis in the osteogenic differentiation of human mesenchymal stem cells

et al. 2008

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Human bone marrow-derived mesenchymal stem cells (hMSCs) have the capacity to differentiate into osteoblasts during osteogenesis. Several studies attempted to identify osteogenesis-related genes in hMSCs. Although HOX genes are known to play a pivotal role in skeletogenesis, their function in the osteogenesis of hMSCs has not yet been investigated in detail. Our aim was to characterize the expression of 37 HOX genes by multiplex RT-PCR to identify the ones most probably involved in osteogenic differentiation. The results showed that the expression patterns of four HOX genes were altered during this process. In particular, the expression levels of HOXC13 and HOXD13 were dramatically changed. Real-time PCR and Western blot analysis were performed in order to further analyze the expression of HOXC13 and HOXD13. The qRT-PCR results showed that transcription of HOXC13 was up-regulated by up to forty times, whereas that of HOXD13 was down-regulated by approximately five times after osteogenic differentiation. The Western blot results for the HOXC13 and HOXD13 proteins also corresponded well with the real-time PCR result. These findings suggest that HOXC13 and HOXD13 might be involved in the osteogenic differentiation of hMSCs.

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KAI1/CD82 suppresses tumor invasion by MMP9 inactivation via TIMP1 up-regulation in the H1299 human lung carcinoma cell line

Cited by 56 publications

References 21 publications

KAI1/CD82 decreases Rac1 expression and cell proliferation through PI3K/Akt/mTOR pathway in H1299 lung carcinoma cells

KAI1/CD82 decreases Rac1 expression and cell proliferation through PI3K/Akt/mTOR pathway in H1299 lung carcinoma cells

Genistein induces the metastasis suppressor kangai-1 which mediates its anti-invasive effects in TRAMP cancer cells

HOX gene analysis in the osteogenic differentiation of human mesenchymal stem cells

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