{"title":"Immunohistochemical Analysis of Nf-κB Expression and its Relation to Apoptosis and Proliferation in Different Odontogenic Tumors","authors":"D. Kh, R. Kasem, Reham A. A. Morsy","doi":"10.3923/IJCR.2017.76.83","DOIUrl":"https://doi.org/10.3923/IJCR.2017.76.83","url":null,"abstract":"","PeriodicalId":90856,"journal":{"name":"International journal of cancer research","volume":"56 1","pages":"76-83"},"PeriodicalIF":0.0,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76282732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Identification of Target Genes in Breast Cancer Pathway using Protein-Protein Interaction Network","authors":"Divya Bafna, Arnold Emerson Isaac","doi":"10.3923/IJCR.2017.51.58","DOIUrl":"https://doi.org/10.3923/IJCR.2017.51.58","url":null,"abstract":"","PeriodicalId":90856,"journal":{"name":"International journal of cancer research","volume":"17 1","pages":"51-58"},"PeriodicalIF":0.0,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79130895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Radiosensitizing Efficacy of Diosmin- Hesperidin Complex Against Ehrlich Solid Carcinoma in Mice, A Potential Role of Histone Deacetylase and Pro-angiogenic Chaperones Targeting","authors":"Mohamed Abd, H. AsmaaAbu-Bakr","doi":"10.3923/IJCR.2017.59.70","DOIUrl":"https://doi.org/10.3923/IJCR.2017.59.70","url":null,"abstract":"","PeriodicalId":90856,"journal":{"name":"International journal of cancer research","volume":"1 1","pages":"59-70"},"PeriodicalIF":0.0,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88604372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Statin Alter Expression of STAT-3 and ß-Catenin Signal Molecules in Gamma Irradiated Model of Carcinoma","authors":"E. Moustafa, N. Thabet, K. Azab","doi":"10.3923/IJCR.2017.41.50","DOIUrl":"https://doi.org/10.3923/IJCR.2017.41.50","url":null,"abstract":"","PeriodicalId":90856,"journal":{"name":"International journal of cancer research","volume":"206 1","pages":"41-50"},"PeriodicalIF":0.0,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80449127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
W. N. Ibrahim, R. A. Wahab, Mohammad Syaiful Bahari Abdull Rasad
Background and Objective: Fibroblast stromal cells actively participates in tumor invasion by secreting matrix metalloproteinases (MMPs) within the tumor microenvironment. Expression of these enzymes is primarily regulated at a transcriptional level via interaction with transcription factors. Among these factors, YB-1 oncogenic factor binds with different nucleic acids to exert its diverse influences. Also it represents an important prognostic indicator in many types of tumors. The aim of this study was to assess the expression of collagenases MMPs (MMP1, MMP8, MMP13) and the cellular proliferation in one of the most invasive types of cancer cell types which is the A375 malignant melanoma cancer cell line using co-culture settings. Also, the study attempted to assess the expression of YB-1 factor and its in vivo interaction with the AP-1 gene promoter sequence. Materials and Methods: The experiment involved growing A375 cells with CCD1079SK fibroblasts cells in co-culture environment. The proliferation of cells was determined using serial trypan blue assays, while the expression of YB-1, MMP1, MMP8 and MMP13 was determined by the use of real-time PCR and western blotting analysis. The potential interaction between YB-1 protein and AP-1 promoter sequence was assessed through chromatin immunoprecipitation (ChIP) assay. SPSS with independent t- test was used to compare cell proliferation and real-time PCR Ct mean values between samples. Results: In co-culture setting, the proliferation of A375 cancer cells was significantly faster than the cells in monoculture setting (5.1×105, 3×105 respectively in day 3) (p<0.05). Also, there was a significant increase in the expression of MMP1 enzyme. YB-1 and MMP8 were significantly expressed more in the A375 cancer cells in comparison with normal fibroblasts cells (p<0.05). Conclusion: The study confirms the role of stromal fibroblasts by enhancing the proliferation of melanoma cancer cells in vitro and increasing the expression of the MMP1 enzyme. In addition, YB-1 factor remains as an important prognostic indicator in cancer that might regulate expression of MMPs without binding to the AP-1 promoter sequence.
{"title":"Expression of collagenases matrix metalloproteinases and YB-1 oncogenic factor in malignant melanoma cancer cells and its regulation by stromal fibroblasts","authors":"W. N. Ibrahim, R. A. Wahab, Mohammad Syaiful Bahari Abdull Rasad","doi":"10.3923/IJCR.2017.17.25","DOIUrl":"https://doi.org/10.3923/IJCR.2017.17.25","url":null,"abstract":"Background and Objective: Fibroblast stromal cells actively participates in tumor invasion by secreting matrix metalloproteinases (MMPs) \u0000within the tumor microenvironment. Expression of these enzymes is primarily regulated at a transcriptional level via interaction with \u0000transcription factors. Among these factors, YB-1 oncogenic factor binds with different nucleic acids to exert its diverse influences. Also \u0000it represents an important prognostic indicator in many types of tumors. The aim of this study was to assess the expression of collagenases \u0000MMPs (MMP1, MMP8, MMP13) and the cellular proliferation in one of the most invasive types of cancer cell types which is the A375 \u0000malignant melanoma cancer cell line using co-culture settings. Also, the study attempted to assess the expression of YB-1 factor and its \u0000in vivo interaction with the AP-1 gene promoter sequence. Materials and Methods: The experiment involved growing A375 cells with \u0000CCD1079SK fibroblasts cells in co-culture environment. The proliferation of cells was determined using serial trypan blue assays, while \u0000the expression of YB-1, MMP1, MMP8 and MMP13 was determined by the use of real-time PCR and western blotting analysis. The potential \u0000interaction between YB-1 protein and AP-1 promoter sequence was assessed through chromatin immunoprecipitation (ChIP) assay. SPSS \u0000with independent t- test was used to compare cell proliferation and real-time PCR Ct mean values between samples. Results: In co-culture \u0000setting, the proliferation of A375 cancer cells was significantly faster than the cells in monoculture setting (5.1×105, 3×105 respectively \u0000in day 3) (p<0.05). Also, there was a significant increase in the expression of MMP1 enzyme. YB-1 and MMP8 were significantly expressed \u0000more in the A375 cancer cells in comparison with normal fibroblasts cells (p<0.05). Conclusion: The study confirms the role of stromal \u0000fibroblasts by enhancing the proliferation of melanoma cancer cells in vitro and increasing the expression of the MMP1 enzyme. In \u0000addition, YB-1 factor remains as an important prognostic indicator in cancer that might regulate expression of MMPs without binding \u0000to the AP-1 promoter sequence.","PeriodicalId":90856,"journal":{"name":"International journal of cancer research","volume":"9 1","pages":"17-25"},"PeriodicalIF":0.0,"publicationDate":"2016-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79794780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"High Level Amplifications of AKT3, SDCCAG8 and SLC35F3 Genes at Chromosomal 1q42.2-44 Region in Non-small Cell Lung Cancer: Early and Prognostic Implications","authors":"J. Kang","doi":"10.3923/IJCR.2017.1.8","DOIUrl":"https://doi.org/10.3923/IJCR.2017.1.8","url":null,"abstract":"","PeriodicalId":90856,"journal":{"name":"International journal of cancer research","volume":"21 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2016-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81205416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. A. Mohammed, Hany R Shabana, T. Sheta, N. Omar, S. Mohammed
{"title":"Vitamin D Receptor Gene Polymorphisms as a Predictive Risk Factor for Hepatocellular Carcinoma Development and Severity in Chronic Hepatitis B","authors":"M. A. Mohammed, Hany R Shabana, T. Sheta, N. Omar, S. Mohammed","doi":"10.3923/IJCR.2017.26.35","DOIUrl":"https://doi.org/10.3923/IJCR.2017.26.35","url":null,"abstract":"","PeriodicalId":90856,"journal":{"name":"International journal of cancer research","volume":"82 1","pages":"26-35"},"PeriodicalIF":0.0,"publicationDate":"2016-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78075965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Siti Aishah Abu Bakar, S. A. T. T-Johari, N. M. Mohamad, M. H. A. Hamid, Mohd Fadhli Mohd Yusoff, A. Ali
Background: Newcastle Disease Virus (NDV) is a negative-sense single stranded RNA virus that causes a Newcastle Disease (ND), a contagious disease of domestic poultry and wild birds characterized by gastro-intestinal, respiratory and nervous signs. Despite the negative effects of NDV to avian species, this virus was reported to possess significant oncolytic activity against mammalian cancerous cells. Methodology: In this study, the antiproliferative and apoptotic effect of NDV strain AF2240 on human promyelocytic leukaemia HL60 cell line were assessed using MTT proliferation assay, microscopic observation, DNA fragmentation, annexin V-FITC assay, caspase-3/7, 8, 9 assays and caspase-3/7, 8, 9 inhibition assays. Results: The proliferation of HL60 cells was inhibited when treated with cytotoxic titers (CD25, CD50 and CD75) of NDV AF2240 for a period of 72 h. Result from microscopic observation showed NDV AF2240 caused inhibition of cell growth and the treated cells exhibited morphological features of apoptosis and a ladder-like pattern of DNA, which is a hallmark of apoptosis. The proportion of cells in early and late apoptosis was quantified by using annexin V-FITC staining and analysed with flow cytometer. The percentage of cells in early apoptosis after treatment with NDV AF2240 at CD50 titer for 24 and 48 h were 16.27±0.25 and 25.93±1.2%, respectively. Late-apoptotic cells were increased from 3.15±0.07 and 6.85±1.05%, respectively. The mechanism of apoptosis through activation of caspases induced by NDV AF2240 was also analysed. The results suggested that apoptosis in NDV-infected tumor cells is dependent on caspase as both iniatiator caspases; caspase 8 and 9 were activated. Activation of caspase-3/7 were also detected in the cells treated with NDV AF2240. Furthermore, apoptosis by NDV AF2240 was effectively inhibited by ZVAD-FMK indicate that NDV AF2240-induced apoptosis is entirely dependent on caspase activation. Conclusion: To conclude, NDV AF2240 was found to have antiproliferative and apoptotic effects on HL60 cells. It has been shown from this study that NDV AF2240 infection resulted in the activation of both intrinsic and extrinsic apoptotic pathways.
{"title":"Antiproliferative and Apoptotic Effect of Newcastle Disease Virus (NDV) Strain AF2240 in Human Promyelocytic Leukemia Cells (HL60)","authors":"Siti Aishah Abu Bakar, S. A. T. T-Johari, N. M. Mohamad, M. H. A. Hamid, Mohd Fadhli Mohd Yusoff, A. Ali","doi":"10.3923/IJCR.2017.9.16","DOIUrl":"https://doi.org/10.3923/IJCR.2017.9.16","url":null,"abstract":"Background: Newcastle Disease Virus (NDV) is a negative-sense single stranded RNA virus that causes a Newcastle Disease (ND), a contagious disease of domestic poultry and wild birds characterized by gastro-intestinal, respiratory and nervous signs. Despite the negative effects of NDV to avian species, this virus was reported to possess significant oncolytic activity against mammalian cancerous cells. Methodology: In this study, the antiproliferative and apoptotic effect of NDV strain AF2240 on human promyelocytic leukaemia HL60 cell line were assessed using MTT proliferation assay, microscopic observation, DNA fragmentation, annexin V-FITC assay, caspase-3/7, 8, 9 assays and caspase-3/7, 8, 9 inhibition assays. Results: The proliferation of HL60 cells was inhibited when treated with cytotoxic titers (CD25, CD50 and CD75) of NDV AF2240 for a period of 72 h. Result from microscopic observation showed NDV AF2240 caused inhibition of cell growth and the treated cells exhibited morphological features of apoptosis and a ladder-like pattern of DNA, which is a hallmark of apoptosis. The proportion of cells in early and late apoptosis was quantified by using annexin V-FITC staining and analysed with flow cytometer. The percentage of cells in early apoptosis after treatment with NDV AF2240 at CD50 titer for 24 and 48 h were 16.27±0.25 and 25.93±1.2%, respectively. Late-apoptotic cells were increased from 3.15±0.07 and 6.85±1.05%, respectively. The mechanism of apoptosis through activation of caspases induced by NDV AF2240 was also analysed. The results suggested that apoptosis in NDV-infected tumor cells is dependent on caspase as both iniatiator caspases; caspase 8 and 9 were activated. Activation of caspase-3/7 were also detected in the cells treated with NDV AF2240. Furthermore, apoptosis by NDV AF2240 was effectively inhibited by ZVAD-FMK indicate that NDV AF2240-induced apoptosis is entirely dependent on caspase activation. Conclusion: To conclude, NDV AF2240 was found to have antiproliferative and apoptotic effects on HL60 cells. It has been shown from this study that NDV AF2240 infection resulted in the activation of both intrinsic and extrinsic apoptotic pathways.","PeriodicalId":90856,"journal":{"name":"International journal of cancer research","volume":"10 1","pages":"9-16"},"PeriodicalIF":0.0,"publicationDate":"2016-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84115547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-15DOI: 10.3923/IJCR.2016.101.108
Muhartono Muhartono, Sutyarso Sutyarso, M. Kanedi
Background: Mucoxinis believed to be a promising anticancer because it is known to inhibit cell proliferation. However, given study on mucoxin still very limited, the mechanism of the substances isolated from leaf extract of Rollinia mucosa in regulating and eliminating cancer cells has not fully understood. This study investigated the mucoxin mechanism in affecting proliferation, expression of p53 and cyclin D1 genes in the T47D breast cancer cells. Materials and Methods: The cell line samples were grouped into four referred to the hour of assays undertaken after mucoxin application, namely hour 0th, 24th, 48th and 72nd. Each group was given mucoxin of six different concentrations namely 0.00 µg mLG 1 as a control, 0.1×10G 3 , 0.5×10G 3 , 1×10G 3 , 5×10G 3 and 10×10 S3 µg mLG with three replications. Cells proliferation assayed by flow cytometry technique using BrDU staining protocol, whereas the expression of p53 and cyclin D1 genes determined by quantitative PCR (qPCR). Results: Cell proliferation in each group significantly reduced by mucoxin treatment. and 10×10 Mucoxin enhance p53 gene expression in 48 h, while the expression of cyclin D1 supressed signifantly by mucoxin of 5×10G S3 µ g mL G in 48 and 72 h. Simple regression analysis showed that cell proliferation decreased with the increase of p53 expression and the suppression of cyclin D1 gene, while p53 expression positively associated to cyclin D1 expression. Conclusion: Mucoxin can 1 decrease the proliferation of T47D breast cancer cells by suppressing the expression of cyclin D1 mediated by p53 gene.
{"title":"Mucoxin (Acetogenin) Inhibits Proliferation of T47D Breast Cancer by Suppressing Expression of Cyclin D1 Mediated by p53","authors":"Muhartono Muhartono, Sutyarso Sutyarso, M. Kanedi","doi":"10.3923/IJCR.2016.101.108","DOIUrl":"https://doi.org/10.3923/IJCR.2016.101.108","url":null,"abstract":"Background: Mucoxinis believed to be a promising anticancer because it is known to inhibit cell proliferation. However, given study on \u0000mucoxin still very limited, the mechanism of the substances isolated from leaf extract of \u0000Rollinia mucosa in regulating and eliminating \u0000cancer cells has not fully understood. This study investigated the mucoxin mechanism in affecting proliferation, expression of p53 and \u0000cyclin D1 genes in the T47D breast cancer cells. Materials and Methods: The cell line samples were grouped into four referred to the hour \u0000of assays undertaken after mucoxin application, namely hour 0th, 24th, 48th and 72nd. Each group was given mucoxin of six different \u0000concentrations namely 0.00 µg mLG \u00001 \u0000 as a control, 0.1×10G \u00003 \u0000, 0.5×10G \u00003 \u0000, 1×10G \u00003 \u0000, 5×10G \u00003 \u0000 and 10×10 \u0000S3 \u0000 µg mLG \u0000 with three replications. \u0000Cells proliferation assayed by flow cytometry technique using BrDU staining protocol, whereas the expression of p53 and cyclin D1 genes \u0000determined by quantitative PCR (qPCR). Results: Cell proliferation in each group significantly reduced by mucoxin treatment. \u0000 and \u000010×10 \u0000Mucoxin enhance p53 gene expression in 48 h, while the expression of cyclin D1 supressed signifantly by mucoxin of 5×10G \u0000S3 \u0000 µ g mL G \u0000 in 48 and 72 h. Simple regression analysis showed that cell proliferation decreased with the increase of p53 expression \u0000and the suppression of cyclin D1 gene, while p53 expression positively associated to cyclin D1 expression. Conclusion: Mucoxin can \u00001 \u0000decrease the proliferation of T47D breast cancer cells by suppressing the expression of cyclin D1 mediated by p53 gene.","PeriodicalId":90856,"journal":{"name":"International journal of cancer research","volume":"12 2 1","pages":"101-108"},"PeriodicalIF":0.0,"publicationDate":"2016-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78334893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-01DOI: 10.3923/IJCR.2016.162.168
S. Sreeja, C. Nair
{"title":"Effect of Hypoxic Cell Sensitizer on Transcription of hif-1α and its Target Genes in Tumor Cells","authors":"S. Sreeja, C. Nair","doi":"10.3923/IJCR.2016.162.168","DOIUrl":"https://doi.org/10.3923/IJCR.2016.162.168","url":null,"abstract":"","PeriodicalId":90856,"journal":{"name":"International journal of cancer research","volume":"105 1","pages":"162-168"},"PeriodicalIF":0.0,"publicationDate":"2016-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80862386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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