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Source: Molecular Carcinogenesis

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Total 68 results found since Jan 2013.

Notch3‐specific inhibition using siRNA knockdown or GSI sensitizes paclitaxel‐resistant ovarian cancer cells
Notch signaling plays an important role in ovarian cancer chemoresistance, which is responsible for recurrence. Gamma‐secretase inhibitor (GSI) is a broad‐spectrum Notch inhibitor, but it has serious side effects. The efficacy of Notch3‐specific inhibition in paclitaxel‐resistant ovarian cancers was assessed in this study, which has not yet been evaluated relative to GSI. To analyze the effect of Notch3‐specific inhibition on paclitaxel‐resistant ovarian cancers, we compared cell viability, apoptosis, cell migration, angiogenesis, cell cycle, and spheroid formation after treatment with either Notch3 siRNA or GS...
Source: Molecular Carcinogenesis - July 24, 2015 Category: Molecular Biology Authors: Haeyoun Kang, Ju‐Yeon Jeong, Ji‐Ye Song, Tae Heon Kim, Gwangil Kim, Jin Hyung Huh, Ah‐Young Kwon, Sang Geun Jung, Hee Jung An Tags: Research Article Source Type: research

(E) ‐2‐methoxy‐4‐(3‐(4‐methoxyphenyl)prop‐1‐en‐1‐yl)phenol suppresses ovarian cancer cell growth via inhibition of ERK and STAT3
This article is protected by copyright. All rights reserved
Source: Molecular Carcinogenesis - March 8, 2017 Category: Molecular Biology Authors: Jie Zheng, Dong Ju Son, Hye Lim Lee, Hee Pom Lee, Tae Hoon Kim, Jung Heun Joo, Young Wan Ham, Wun Jae Kim, Jae Kyung Jung, Sang ‐Bae Han, Jin Tae Hong Tags: RESEARCH ARTICLE Source Type: research

Regulation of HIF‐1 alpha by the proprotein convertases furin and PC7 in human squamous carcinoma cells
Proprotein convertases (PC), a family of serine proteases, process cancer‐related substrates such as growth factors, growth factor receptors, cell adhesion molecules, metalloproteinases, etc. HIF‐1α is a major transcription factor involved in tumorigenesis by sensing intratumoral hypoxia. Furin (PCSK3) is one of the numerous target genes regulated by HIF‐1α transactivation and its distribution into endosomal compartments and onto the cell surface can be triggered by hypoxia via HIF‐1α. siRNAs to knockdown PCs were transfected into cells alone or in combination with different drug treatments. Protein and RNA expr...
Source: Molecular Carcinogenesis - January 1, 2014 Category: Molecular Biology Authors: Jian Fu, Jirong Zhang, Yulan Gong, Courtney Lyons Testa, Andres J. Klein‐Szanto Tags: Research Article Source Type: research

Paracrine CCL20 loop induces epithelial‐mesenchymal transition in breast epithelial cells
The objective of this study was to investigate the hypothesis that CCL20 modulated the epithelial‐mesenchymal transition (EMT) of primarily cultured healthy breast epithelial cells and the angiogenesis in areas adjacent to the tumor. Key results showed that CCL20 (a) down‐regulated E‐cadherin and ZO‐1; (b) up‐regulated N‐cadherin, vimentin, and Snail expressions; (c) increased mRNA and secretion of VEGF and (d) increased angiogenic micro vessel sprouting. Thus, the signal transduction pathways evoked by CCL20 were investigated. We showed that NF‐kB p65 down‐regulation (by small interfering RNA, siRNA) rever...
Source: Molecular Carcinogenesis - July 8, 2015 Category: Molecular Biology Authors: S. Marsigliante, C. Vetrugno, A. Muscella Tags: Research Article Source Type: research

Anticancer activity of fish oils against human lung cancer is associated with changes in formation of PGE2 and PGE3 and Alteration of Akt Phosphorylation
Abstract The beneficial effects of omega‐3 fatty acids are believed to be due in part to selective alteration of arachidonate metabolism that involves cyclooxygenase (COX) enzymes. Here we investigated the effect of eicosapentaenoic acid (EPA) on the proliferation of human non‐small cell lung cancer A549 (COX‐2 over‐expressing) and H1299 (COX‐2 null) cells as well as their xenograft models. While EPA inhibited 50% of proliferation of A549 cells at 6.05 µM, almost 80 µM of EPA was needed to reach similar levels of inhibition of H1299 cells. The formation of prostaglandin (PG)E3 in A549 cells was almost three...
Source: Molecular Carcinogenesis - January 31, 2013 Category: Molecular Biology Authors: Peiying Yang, Carrie Cartwright, Diana Chan, Jibin Ding, Edward Felix, Yong Pan, Jihai Pang, Patrea Rhea, Keith Block, Susan M. Fischer, Robert A. Newman Tags: Research Article Source Type: research

Thromboxane A2 receptor‐mediated release of matrix metalloproteinase‐1 (MMP‐1) induces expression of monocyte chemoattractant protein‐1 (MCP‐1) by activation of protease‐activated receptor 2 (PAR2) in A549 human lung adenocarcinoma cells
Abstract Matrix metalloproteinases (MMPs) and monocyte chemoattractant protein‐1 (MCP‐1, CCL2) are known to be upregulated in many tumors. Their roles in tumor invasion and metastasis are being uncovered. How they are related to each other and involved in tumor progression remains to be determined. Earlier it was reported that I‐BOP‐initiated activation of thromboxane A2 receptor (TP) induced the release of MMP‐1, MMP‐3, and MMP‐9 from lung cancer A549 cells overexpressing TPα (A549‐TPα). Herein it was found that MMP‐1, but not MMP‐3 or MMP‐9, induced the expression of MCP‐1 in A549 cells. Conditi...
Source: Molecular Carcinogenesis - March 8, 2013 Category: Molecular Biology Authors: Xiuling Li, Hsin‐Hsiung Tai Tags: Research Article Source Type: research

CD44/cellular prion protein interact in multidrug resistant breast cancer cells and correlate with responses to neoadjuvant chemotherapy in breast cancer patients
Abstract Multidrug resistance (MDR) is one of the most important factors leading to chemotherapeutic failure in patients with breast cancer. The invasive/metastatic ability of MDR cells is strengthened compared with their parental cells. However, the mechanisms underlying MDR have not been fully elucidated. We found that CD44 and the cellular prion protein (PrPc) were both overexpressed in MDR cells (MCF7/Adr and H69AR). Subsequently, we chose the human breast cancer cell line MCF7/Adr, which is resistant to adriamycin, for further research. We discovered that PrPc physically and functionally interacted with CD44. The knoc...
Source: Molecular Carcinogenesis - May 16, 2013 Category: Molecular Biology Authors: Yuanyuan Cheng, Lili Tao, Jiawen Xu, Qingquan Li, Juan Yu, Yiting Jin, Qi Chen, Zude Xu, Qiang Zou, Xiuping Liu Tags: Research Article Source Type: research

PPARδ deficiency disrupts hypoxia‐mediated tumorigenic potential of colon cancer cells
Peroxisome proliferator‐activated receptor (PPAR) δ is highly expressed in colon epithelial cells and closely linked to colon carcinogenesis. However, the role of PPARδ in colon cancer cells in a hypoxic tumor microenvironment is not fully understood. We found that expression of the tumor‐promoting cytokines, IL‐8 and VEGF, induced by hypoxia (<1% O2) and deferoxamine (a hypoxia mimetic) was significantly attenuated in PPARδ‐deficient HCT116 colon cancer cells. Consequently, PPARδ‐knockout colon cancer cells exposed to hypoxia and deferoxamine failed to stimulate endothelial cell vascularization and macrop...
Source: Molecular Carcinogenesis - March 9, 2014 Category: Molecular Biology Authors: Eunshil Jeong, Jung Eun Koo, Sang Hyeon Yeon, Mi‐Kyoung Kwak, Daniel H. Hwang, Joo Young Lee Tags: Research Article Source Type: research

Erbb2 up‐regulation of ADAM12 expression accelerates skin cancer progression
Solar ultraviolet (UV) radiation can cause severe damage to the skin and is the primary cause of most skin cancer. UV radiation causes DNA damage leading to mutations and also activates the Erbb2/HER2 receptor through indirect mechanisms involving reactive oxygen species. We hypothesized that Erbb2 activation accelerates the malignant progression of UV‐induced skin cancer. Following the induction of benign squamous papillomas by UV exposure of v‐rasHa transgenic Tg.AC mice, mice were treated topically with the Erbb2 inhibitor AG825 and tumor progression monitored. AG825 treatment reduced tumor volume, increased tumor r...
Source: Molecular Carcinogenesis - May 5, 2014 Category: Molecular Biology Authors: Velidi H. Rao, Kristen Vogel, Jodi K. Yanagida, Nitin Marwaha, Amrit Kandel, Carol Trempus, Susan K. Repertinger, Laura A. Hansen Tags: Research Article Source Type: research

Targeting Fyn in Ras‐transformed cells induces F‐actin to promote adherens junction‐mediated cell–cell adhesion
Fyn, a member of the Src family kinases (SFK), is an oncogene in murine epidermis and is associated with cell–cell adhesion turnover and induction of cell migration. Additionally, Fyn upregulation has been reported in multiple tumor types, including cutaneous squamous cell carcinoma (cSCC). Introduction of active H‐Ras(G12V) into the HaCaT human keratinocyte cell line resulted in upregulation of Fyn mRNA (200‐fold) and protein, while expression of other SFKs remained unaltered. Transduction of active Ras or Fyn was sufficient to induce an epithelial‐to‐mesenchymal transition in HaCaT cells. Inhibition of Fyn acti...
Source: Molecular Carcinogenesis - June 29, 2014 Category: Molecular Biology Authors: Sarah E. Fenton, Kelli A. Hutchens, Mitchell F. Denning Tags: Research Article Source Type: research

Zbed3 contributes to malignant phenotype of lung cancer via regulating β‐catenin and P120‐catenin 1
Our previous studies indicate that abnormal expression of several Wnt signaling molecules including Axin, Dvl and β‐catenin are involved in proliferation, invasion and metastasis of lung cancer. Zbed3 was found to inhibit function of Axin‐GSK3β complex and thus lead to accumulation of β‐catenin in NIH3T3 and HEK293T cells. However its function in malignant tumors is largely unknown. Here we investigate the clinico‐pathological significance of Zbed3 expression and its function in non‐small cell lung cancer. We use immunohistochemistry and Western blotting to examine Zbed3 expression in non‐small cell lung can...
Source: Molecular Carcinogenesis - September 27, 2014 Category: Molecular Biology Authors: Chuifeng Fan, Guiyang Jiang, Xiupeng Zhang, Yuan Miao, Xuyong Lin, Lan Luan, Zhonghai Xu, Yijun Zhang, Huanyu Zhao, Di Liu, Enhua Wang Tags: Research Article Source Type: research

β‐catenin regulates c‐Myc and CDKN1A expression in breast cancer cells
In this study, we found that c‐Myc is highly expressed in the basal‐like subtype by microarray analyses and immunohistochemical staining. After silencing β‐catenin using siRNA, c‐Myc expression was decreased in non‐basal‐like breast cancer cells. In contrast, c‐Myc mRNA and protein expression were up‐regulated in the basal‐like breast cancer cell lines. Decreased c‐Myc promoter activity was observed after inhibiting β‐catenin by siRNA in non‐basal‐like breast cancer cells; however, inhibition of β‐catenin or over‐expression of dominant‐negative LEF1 had no effect on c‐Myc promoter activ...
Source: Molecular Carcinogenesis - February 8, 2015 Category: Molecular Biology Authors: Jinhua Xu, Yinghua Chen, Dezheng Huo, Andrey Khramtsov, Galina Khramtsova, Chunling Zhang, Kathleen H. Goss, Olufunmilayo I. Olopade Tags: Research Article Source Type: research

TGFβ induces epithelial‐mesenchymal transition of thyroid cancer cells by both the BRAF/MEK/ERK and Src/FAK pathways
The epithelial‐mesenchymal transition (EMT) is a crucial process in tumour progression, by which epithelial cells acquire a mesenchymal phenotype, increasing its motility and the ability to invade distant sites. Here, we describe the molecular mechanisms by which V600EBRAF, TGFβ and the Src/FAK complex cooperatively regulate EMT induction and cell motility of anaplastic thyroid cancer cells. Analysis of EMT marker levels reveals a positive correlation between TGFβ and Snail expression, with a concomitant downregulation of E‐cadherin, accompanied by an increase of cell migration and invasion. Furthermore, we show that...
Source: Molecular Carcinogenesis - September 22, 2015 Category: Molecular Biology Authors: Pablo Baquero, Eva Jiménez‐Mora, Adrián Santos, Marina Lasa, Antonio Chiloeches Tags: Research Article Source Type: research

TGF β induces epithelial‐mesenchymal transition of thyroid cancer cells by both the BRAF/MEK/ERK and Src/FAK pathways
The epithelial‐mesenchymal transition (EMT) is a crucial process in tumour progression, by which epithelial cells acquire a mesenchymal phenotype, increasing its motility and the ability to invade distant sites. Here, we describe the molecular mechanisms by which V600EBRAF, TGFβ and the Src/FAK complex cooperatively regulate EMT induction and cell motility of anaplastic thyroid cancer cells. Analysis of EMT marker levels reveals a positive correlation between TGFβ and Snail expression, with a concomitant downregulation of E‐cadherin, accompanied by an increase of cell migration and invasion. Furthermore, we show that...
Source: Molecular Carcinogenesis - September 20, 2015 Category: Molecular Biology Authors: Pablo Baquero, Eva Jim énez‐Mora, Adrián Santos, Marina Lasa, Antonio Chiloeches Tags: Article Source Type: research

The role of metastasis ‐associated in colon cancer 1 (MACC1) in endometrial carcinoma tumorigenesis and progression
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Source: Molecular Carcinogenesis - December 19, 2016 Category: Molecular Biology Authors: Shuo Chen, Zhi ‐Hong Zong, Dan‐dan Wu, Kai‐Xuan Sun, Bo‐Liang Liu, Yang Zhao Tags: Research Article Source Type: research