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Source: Molecular Carcinogenesis
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Total 68 results found since Jan 2013.
Expression, modulation, and clinical correlates of the autophagy protein Beclin ‐1 in esophageal adenocarcinoma
We report for the first time, loss of Beclin‐1, a key mediator of autophagy, was significantly linked to prognostic factors in EAC. Specifically, Beclin‐1 expression loss occurred in 49.0% of EAC patients versus 4.8% of controls. There was a significant inverse correlation between loss of Beclin‐1 with histologic grade and tumor stage supporting a tumor suppressive role for Beclin‐1. Autophagy modulation linked to cell death was examined in EAC cell lines following treatment with a proanthocyanidin‐rich cranberry extract, C‐PAC, and the commonly used autophagy inducer, rapamycin. C‐PAC induced Beclin‐1‐in...
Source: Molecular Carcinogenesis - November 18, 2015 Category: Molecular Biology Authors: Katherine M. Weh, Amy B. Howell, Laura A. Kresty Tags: Brief Communication 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
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
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
Par‐4 dependent modulation of cellular β‐catenin by medicinal plant natural product derivative 3‐azido Withaferin A
This study, for the first time, reveals 3‐AWA treatment consistently sequestered nuclear β‐catenin and augmented its cytoplasmic pool as evidenced by reducing β‐catenin transcriptional activity in these cells. Moreover, 3‐AWA treatment triggered robust induction of pro‐apoptotic intracellular Par‐4, attenuated Akt activity and rescued Phospho‐GSK3β (by Akt) to promote β‐catenin destabilization. Further, our in vitro studies demonstrate that 3‐AWA treatment amplified E‐cadherin expression along with sharp downregulation of c‐Myc and cyclin D1 proteins. Strikingly, endogenous Par‐4 knock down by s...
Source: Molecular Carcinogenesis - May 12, 2015 Category: Molecular Biology Authors: Hina Amin, Debasis Nayak, Reyaz ur Rasool, Souneek Chakraborty, Anmol Kumar, Khalid Yousuf, Parduman Raj Sharma, Zabeer Ahmed, Neelam Sharma, Asmita Magotra, Debaraj Mukherjee, Lekha Dinesh Kumar, Anindya Goswami Tags: Research Article Source Type: research
LW‐213 induces G2/M cell cycle arrest through AKT/GSK3β/β‐catenin signaling pathway in human breast cancer cells
In conclusion, we found LW‐213 exerts its anticancer effect on cell proliferation and cell cycle through repression of Akt/Gsk3β/β‐catenin signaling pathway. LW‐213 could be a potential candidate for anticancer drug development. © 2015 Wiley Periodicals, Inc.
Source: Molecular Carcinogenesis - May 6, 2015 Category: Molecular Biology Authors: Li Zhao, Han‐Chi Miao, Wen‐Jun Li, Yang Sun, Shao‐liang Huang, Zhi‐Yu Li, Qing‐Long Guo Tags: Research Article Source Type: research
Anti‐cancer effect of N‐(3,5‐bis(trifluoromethyl)phenyl)‐5‐chloro‐2,3‐dihydronaphtho1,2‐bfuran‐2‐carboxamide, a novel synthetic compound
In this study, we investigated whether N‐(3,5‐bis(trifluoromethyl)phenyl)‐5‐chloro‐2,3‐dihydronaphtho[1,2‐b]furan‐2‐carboxamide (NHDC), a novel synthetic naphthofuran compound inhibits liver tumor growth through activation of HNF 4α. Treatment with different concentrations (1–10.8 µM) of NHDC for various periods (0–72 h) inhibited liver cancer cells (HepG2, Hep3B) growth as well as colony formation followed by induction of apoptosis in a concentration dependent manner. NHDC also induced expression of the apoptosis regulating genes as well as inhibiting the action of STAT3. These inhibitory effec...
Source: Molecular Carcinogenesis - April 11, 2015 Category: Molecular Biology Authors: Sun Mi Kwon, Yu Yeon Jung, Chul Ju Hwang, Mi Hee Park, Na Young Yoon, Tae Myung Kim, Ji Myung Yu, Dae Hwan Kim, Doo Won Seo, Hyu Seok Youn, Hyun Ok Seo, In Sung Chung, Sang Bae Han, Bang Yeon Hwang, Hwan‐Soo Yoo, Jae‐Kyung Jung, Heesoon Lee, Jin Tae H Tags: Research Article Source Type: research
Antitumor effects of interleukin‐6 (IL‐6)/interleukin‐6 receptor (IL‐6R) signaling pathway inhibition in clear cell carcinoma of the ovary
In this study, we aim to clarify whether IL‐6/IL‐6R mediated signaling pathway could have clinical relations with CCC and to evaluate inhibitory effects of the pathway on CCC carcinogenesis. A total of 84 CCC cases collected from primary surgical specimens were evaluated by the immunohistochemical analysis for IL‐6R and phosphorylated Stat3 (pStat3), and we found that high IL‐6R expression correlated with poor patient survival both by the univariate and multivariate analyses, suggesting that IL‐6/IL‐6R signaling pathway could be implicated in the progression of CCC. We further investigated the effects of IL‐6...
Source: Molecular Carcinogenesis - April 10, 2015 Category: Molecular Biology Authors: Nozomu Yanaihara, Yukihiro Hirata, Noriko Yamaguchi, Yukiko Noguchi, Misato Saito, Chie Nagata, Satoshi Takakura, Kyosuke Yamada, Aikou Okamoto Tags: Research Article Source Type: research
Microcystin‐LR promotes migration and invasion of colorectal cancer through matrix metalloproteinase‐13 up‐regulation
Microcystin‐LR (MC–LR) is an environmental toxin from blooms of cyanobacteria and it has been shown to be one of the environmental carcinogens for the progression of colorectal carcinoma. However, there is no direct evidence that MC–LR can induce colorectal cancer migration and invasion. In the present study, 0.04 or 40 µg/kg/d (human tolerable daily intake value of MC–LR) MC–LR treatment was observed to induce Matrix Metalloproteinase‐13 (MMP‐13) expression in tumor tissues and local invasion in DLD‐1 xenograft model. The results are consistent with those of cell test showing that MC–LR treatment enha...
Source: Molecular Carcinogenesis - March 19, 2015 Category: Molecular Biology Authors: Chen Miao, Yan Ren, Meng Chen, Zhen Wang, Ting Wang Tags: Research Article Source Type: research
Embigin is overexpressed in pancreatic ductal adenocarcinoma and regulates cell motility through epithelial to mesenchymal transition via the TGF‐β pathway
Embigin is a member of the immunoglobulin superfamily and encodes a transmembrane glycoprotein. There have been reports of Embigin involvement in neuromuscular junction formation and plasticity; however, the molecular functions of Embigin in other organs are unknown. Our aim was to investigate the possible role of Embigin in pancreatic cancer. In pancreatic ductal adenocarcinoma tissues, Embigin expression was higher than that in normal pancreatic tissues. Immunohistochemical analysis revealed expression of Embigin in pancreatic cancer cells, as well as expression of monocarboxylate transporter 2 (MCT2) in cancer tissues. ...
Source: Molecular Carcinogenesis - March 15, 2015 Category: Molecular Biology Authors: Dawoon E. Jung, Jeong Mi Kim, Chanyang Kim, Si Young Song Tags: Research Article Source Type: research
Involvement of cysteine‐rich protein 61 in the epidermal growth factor‐induced migration of human anaplastic thyroid cancer cells
In this study, we found that EGF treatment induced cell migration, stress fiber formation, Cyr61 mRNA and protein expressions, and Cyr61 protein secretion in ATC cells. The recombinant Cyr61 protein significantly induced cell migration; however, inhibition of Cyr61 activity by a Cyr61‐specific antibody abrogated EGF‐induced cell migration. EGF treatment also affected epithelial‐to‐mesenchymal transition (EMT)‐related marker protein expression, as evidenced by an increase in vimentin and a decrease in E‐cadherin expression. Inhibition of Cyr61 expression by Cyr61 siRNA decreased cell migration and reversed the E...
Source: Molecular Carcinogenesis - March 14, 2015 Category: Molecular Biology Authors: Li‐Han Chin, Sung‐Po Hsu, Wen‐Bin Zhong, Yu‐Chih Liang Tags: Research Article Source Type: research
Sonic hedgehog (Shh) signaling promotes tumorigenicity and stemness via activation of epithelial‐to‐mesenchymal transition (EMT) in bladder cancer
Activation of the sonic hedgehog (Shh) signaling pathway controls tumorigenesis in a variety of cancers. Here, we show a role for Shh signaling in the promotion of epithelial‐to‐mesenchymal transition (EMT), tumorigenicity, and stemness in the bladder cancer. EMT induction was assessed by the decreased expression of E‐cadherin and ZO‐1 and increased expression of N‐cadherin. The induced EMT was associated with increased cell motility, invasiveness, and clonogenicity. These progression relevant behaviors were attenuated by treatment with Hh inhibitors cyclopamine and GDC‐0449, and after knockdown by Shh‐siRNA,...
Source: Molecular Carcinogenesis - March 1, 2015 Category: Molecular Biology Authors: S.S. Islam, R.B. Mokhtari, A.S. Noman, M. Uddin, M.Z. Rahman, M.A. Azadi, A. Zlotta, T. van der Kwast, H. Yeger, W.A. Farhat 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
Elimination of ALDH+ Breast Tumor Initiating Cells by Docosahexanoic Acid and/or Gamma Tocotrienol Through SHP‐1 Inhibition of STAT3 Signaling
Study investigated the ability of docosahexaenoic acid (DHA) alone and in combination with gamma‐tocotrienol (γT3) to eliminate aldehyde dehydrogenase positive (ALDH+) cells and to inhibit mammosphere formation, biomarker and functional assay for tumor initiating cells (TICs), respectively, in human triple negative breast cancer cells (TNBCs), and investigated possible mechanisms of action. DHA upregulated Src homology region 2 domain‐containing protein tyrosine phosphatase‐1 (SHP‐1) protein levels and suppressed levels of phosphorylated signal transducer and activator of transcription‐3 (pStat3) and its downstr...
Source: Molecular Carcinogenesis - February 3, 2015 Category: Molecular Biology Authors: Ailian Xiong, Weiping Yu, Yaobin Liu, Bob G. Sanders, Kimberly Kline Tags: Research Article Source Type: research
