Immunological aspects of REIC/Dkk-3 in monocyte differentiation and tumor regression

Watanabe, Masami; Kashiwakura, Yuji; Huang, Peng; Ochiai, Kazuhiko; Futami, Junichiro; Li, Shun Ai; Takaoka, Munenori; Nasu, Yasutomo; Sakaguchi, Masakiyo; Huh, Nam; Kumon, Hiromi

doi:10.3892/ijo_00000191

Cited by 47 publications

(96 citation statements)

References 15 publications

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“…The suppression of tumor growth was further confirmed in an in vivo situation using an orthotopic tumor model. These phenomena were consistent with other published studies (3,5,9,10,(15)(16)(17)(18), showing that ectopic expression of REIC/ Dkk-3 induces apoptosis and inhibits cell proliferation in various cancer cells. Therefore, the lack or absence of endogenous REIC/Dkk-3 expression in RM9 cancer cells seems to be important for the cellular effects induced by the REIC/Dkk-3 overexpression.…”

Section: Discussionsupporting

confidence: 93%

REIC/Dkk-3 stable transfection reduces the malignant phenotype of mouse prostate cancer RM9 cells

Chen

Watanabe²,

Huang³

et al. 2009

Int J Mol Med

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Abstract. The reduced expression in immortalized cells (REIC)/Dickkopf (Dkk)-3, a member of the Dkk gene family, is a tumor suppressor in a broad range of cancers. REIC/Dkk-3 transfected stable clones of mouse prostate cancer RM9 cells (RM9-REIC) and the empty vector-transfected control clone cells (RM9-EV) were established. Clones were used to evaluate the anti-cancer effects and a proteomics analysis of REIC/Dkk-3 continuous expression was performed. The RM9-REIC cells show a feeble appearance and the cell membrane shows irregular buds known as blebs. In vitro cell proliferation was significantly suppressed in RM9-REIC clones in comparison to the control. The apoptosis assay was done under standard culture conditions and RM9-REIC showed a higher incidence of apoptosis. The RM9-EV and RM9-REIC cells were orthotopically implanted into a C57BL/6 mouse prostate. After 2 weeks, the tumor growth was significantly inhibited in RM9-REIC cells in comparison to the control. Two-dimensional gel electrophoresis was used to examine the modification of protein expression by the gene transfection. The analysis with mass spectrometry disclosed that expression of peroxiredoxin-1, GST-P1, transgelin-2, MRP-L12, ARD, GRP78 and Sorcin were increased and eEF1A-1 and cyclophilin-40 protein were decreased in RM9-REIC cells. Therefore, REIC/Dkk-3 stable transfectants show a reduction of malignancy in mouse prostate cancer RM9 cells in vitro and in vivo. The result of the proteomics analysis might provide important clues to clarify the anti-cancer molecular mechanism of REIC/Dkk-3 gene transfer.

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Section: Discussionsupporting

confidence: 93%

REIC/Dkk-3 stable transfection reduces the malignant phenotype of mouse prostate cancer RM9 cells

Chen

Watanabe²,

Huang³

et al. 2009

Int J Mol Med

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show abstract

“…Dulbecco's modified Eagle's medium (DMEM; Invitrogen, Carlsbad, CA), RPMI-1640 and HAM'S F-12 K medium (Nissui, Tokyo, Japan) were used for the culture of human cancerous and non-cancerous cell lines. The cell lines were grown in the medium supplemented with 10% fetal bovine serum (FBS; Biowest, Nuaille, France), as previously described (14).…”

Section: Methodsmentioning

confidence: 99%

Advanced two-step transcriptional amplification as a novel method for cancer-specific gene expression and imaging

et al. 2011

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Abstract. The two-step transcriptional amplification (TSTA) system was previously reported to enhance the tissue-specific gene expression driven by weak promoters, but the enhancement of the gene expression is limited to use in in vitro and in vivo experimental situations. To achieve robust tissuespecific gene expression using the TSTA system, we developed an advanced TSTA system which includes polyglutamines and rat glucocorticoid receptor sequences between the GAL4 and VP16 sequences in the region of the first step of transcription. We evaluated the advanced TSTA system as a method to enhance the human telomerase reverse transcriptase (hTERT) promoter-driving cancer-specific transcription in various cancer cell lines. As a result, the advanced TSTA enhanced cancer-specific luciferase gene expression in all of the examined cancer cell lines, when compared with both the one-step and conventional TSTA systems (an ~6-and ~17-fold enhancement, respectively). Notably, the enhancement of the hTERT driven expression by the conventional TSTA system was modest and even inferior to the one-step system in several cancer cell lines. We then constructed a luciferase gene encoding the adenoassociated virus vector in which the hTERT promoter-mediated expression was driven by the advanced TSTA or control systems. In an orthotopic liver tumor model, mice were treated with the vector via tail vein injection. An optical imaging device was used to visualize the in vivo luciferase expression in the orthotopic tumor. The advanced TSTA system significantly enhanced the luciferase expression compared with the one-step and conventional TSTA systems (18.0±1.0-and 15.9±0.85-fold gain, respectively). Therefore, the advanced TSTA system significantly improves hTERT-dependent cancer-specific gene expression both in vitro and in vivo when compared with the previous systems. Since the advanced TSTA method can also be applied to other site-specific gene expression systems using tissue-specific promoters, this approach is expected to become a valuable tool enabling in vivo site-specific targeting in the field of gene therapy and molecular imaging.

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“…The precipitates were analyzed by a Western blotting analysis with the anti-V5 mouse monoclonal antibody (Invitrogen, Cat.No. R96025), as previously described [12].…”

Section: Immunoprecipitationmentioning

confidence: 99%

Tumor suppressor REIC/Dkk-3 interacts with the dynein light chain, Tctex-1

Ochiai

Watanabe

Ueki

et al. 2011

Biochemical and Biophysical Research Communications

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Immunological aspects of REIC/Dkk-3 in monocyte differentiation and tumor regression

Cited by 47 publications

References 15 publications

REIC/Dkk-3 stable transfection reduces the malignant phenotype of mouse prostate cancer RM9 cells

REIC/Dkk-3 stable transfection reduces the malignant phenotype of mouse prostate cancer RM9 cells

Advanced two-step transcriptional amplification as a novel method for cancer-specific gene expression and imaging

Tumor suppressor REIC/Dkk-3 interacts with the dynein light chain, Tctex-1

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