Gonadotropin-releasing hormone-agonist induces apoptosis of human granulosa-luteal cells &lt;i&gt;via&lt;/i&gt; caspase-8, -9 and -3, and poly-(ADP-ribose)-polymerase cleavage

Park, Eun Joo; Shin, JJung Whan; Seo, Yeon‐Soo; Kim, Dae Wun; Hong, Seo Yoo; Park, Won Il; Kang, Byung Moon

doi:10.5582/bst.2011.v5.3.120

Cited by 23 publications

(14 citation statements)

References 44 publications

(46 reference statements)

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“…The bound antibodies were visualized using an enhanced chemiluminescence reagent (Millipore, Billerica, MA) and quantified by densitometry using ChemiDoc XRS+ image analyzer (Bio‐Rad, Hercules, CA). Densitometric analyses of bands were adjusted with β‐actin functioning as a loading control 24. Experiments were performed in triplicate separately.…”

Section: Methodsmentioning

confidence: 99%

Chemoprevention of intestinal adenomatous polyposis by acetyl‐11‐keto‐beta‐boswellic acid in APC^Min/+ mice

Liu

Gao

Cui

et al. 2012

Intl Journal of Cancer

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Acetyl-11-keto-beta-boswellic acid (AKBA) is a derivative of boswellic acid, which is an active component of the gum resin of Boswellia serrata. AKBA has been used as an adjuvant medication for treatment of inflammatory diseases. In this study, we aimed to evaluate the efficacy of AKBA as a chemopreventive agent against intestinal adenomatous polyposis in the adenomatous polyposis coli multiple intestinal neoplasia (APC Min/1 ) mouse model. APC Min/1 mice were administered AKBA by p.o. gavage for 8 consecutive weeks. The mice were sacrificed and the number, size and histopathology of intestinal polyps were examined by light microscopy. AKBA decreased polyp numbers by 48.9% in the small intestine and 60.4% in the colon. An even greater AKBA effect was observed in preventing the malignant progression of these polyps. The number of large (>3 cm) colonic polyposis was reduced by 77.8%. Histopathologic analysis demonstrated a significant reduction in the number of dysplastic cells and in the degree of dysplasia in each polyp after AKBA treatment. There was no evidence of high grade dysplasia or intramucosal carcinoma in any of the polyps examined within the treated group. More interestingly, interdigitated normal appearing intestinal villi were observed in the polyps of the treated group. During the course of the study, AKBA was well tolerated by the mice with no obvious signs of toxicity. Results from immunohistochemical staining, Western blotting and enzyme-linked immunosorbent assay indicated that the chemopreventive effect of AKBA was attributed to a collection of activities including antiproliferation, apoptosis induction, antiangiogenesis and anti-inflammation. AKBA was found to exert its chemopreventive action through the inhibition of the Wnt/b-catenin and NF-jB/cyclooxygenase-2 signaling pathways. Our findings suggest that AKBA could be a promising regimen in chemoprevention against intestinal tumorigenesis.Colorectal cancer (CRC) is one of the leading causes of worldwide morbidity and mortality due to cancer. At least, three major forms of CRC have been described: hereditary, sporadic and colitis-associated CRC. Lifestyle factors such as diet, exercise and obesity are considered to be linked to CRC risk. CRCs are known to develop through a series of histological events, called the ''adenoma-carcinoma'' sequence. Thus, adenomatous polyps or adenomas are believed to be major precursors of CRC. 1,2 Almost half of the population will develop at least one benign adenomatous colonic polyp, and less than 3% of these cases will progress into CRCs. 3 Surgical resection and/or adjuvant therapy of early CRCs lead to a 90% 5-year survival rate. Unfortunately, only about 37% of patients are diagnosed at this early stage. 4 Thus, in addition to improving therapeutic options; better cancer prevention strategies are needed.The mutation of a tumor suppressor gene, adenomatous polyposis coli (APC), is the initiating event in both familial adenomatous polyposis (FAP) and the majority of sporadic CRC patients. Recent reports i...

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Section: Methodsmentioning

confidence: 99%

Chemoprevention of intestinal adenomatous polyposis by acetyl‐11‐keto‐beta‐boswellic acid in APC^Min/+ mice

Liu

Gao

Cui

et al. 2012

Intl Journal of Cancer

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“…The bound antibodies were visualized using an enhanced chemiluminescence reagent (Millipore, USA) and quantified by densitometry using ChemiDoc XRS+ image analyzer (Bio-Rad, USA). Densitometric analyses of bands were adjusted with β-actin as loading control [23]. Triplicate experiments with triplicate samples were performed.…”

Section: Methodsmentioning

confidence: 99%

Inhibition of Intestinal Adenoma Formation in APCMin/+ Mice by Riccardin D, a Natural Product Derived from Liverwort Plant Dumortiera hirsuta

et al. 2012

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BackgroundMutation of tumor suppressor gene, adenomatous polyposis coli (APC), is the primary molecular event in the development of most intestinal carcinomas. Animal model with APC gene mutation is an effective tool for study of preventive approaches against intestinal carcinomas. We aimed to evaluate the effect of Riccardin D, a macrocyclic bisbibenzyl compound, as a chemopreventive agent against intestinal adenoma formation in APCMin/+ mice.Methods APCMin/+ mice were given Riccardin D by p.o. gavage for 7 weeks. Mice were sacrificed, and the number, size and histopathology of intestinal polyps were examined under a microscope. We performed immunohistochemical staining, western blotting, reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) in intestinal polyps to investigate the mechanism of chemopreventive effect of Riccardin D.ResultsRiccardin D treatment resulted in a significant inhibition of intestinal adenoma formation, showing a reduction of polyp number by 41.7%, 31.1% and 44.4%, respectively, in proximal, middle and distal portions of small intestine. The activity of Riccardin D against polyp formation was more profound in colon, wherein Riccardin D decreased polyp number by 79.3%. Size distribution analysis revealed a significant reduction in large-size polyps (2–3 mm) by 40.0%, 42.5% and 33.3%, respectively, in proximal, middle and distal portions of small intestine, and 77.8% in colon. Histopathological analysis of the intestinal polyps revealed mostly hyperplastic morphology without obvious dysplasia in Riccardin D-treated mice. Molecular analyses of the polyps suggested that the inhibitory effect of Riccardin D on intestinal adenoma formation was associated with its abilities of reduction in cell proliferation, induction of apoptosis, antiangiogenesis, inhibition of the Wnt signaling pathway and suppression of inflammatory mediators in polyps.ConclusionsOur results suggested that Riccardin D exerts its chemopreventive effect against intestinal adenoma formation through multiple mechanisms including anti-proliferative, apoptotic, anti-angiogenic and anti-inflammatory activity.

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“…The data is expressed as the relative density of the protein normalized to ␤-actin. The percentages of inhibition were estimated by comparison to vehicle control cells/H460 xenografts (100%) [21].…”

Section: Western Blotting Assaymentioning

confidence: 99%

Inhibitory effect of riccardin D on growth of human non-small cell lung cancer: In vitro and in vivo studies

Xue

Sun

et al. 2012

Lung Cancer

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Gonadotropin-releasing hormone-agonist induces apoptosis of human granulosa-luteal cells <i>via</i> caspase-8, -9 and -3, and poly-(ADP-ribose)-polymerase cleavage

Cited by 23 publications

References 44 publications

Chemoprevention of intestinal adenomatous polyposis by acetyl‐11‐keto‐beta‐boswellic acid in APC^Min/+ mice

Chemoprevention of intestinal adenomatous polyposis by acetyl‐11‐keto‐beta‐boswellic acid in APC^Min/+ mice

Inhibition of Intestinal Adenoma Formation in APCMin/+ Mice by Riccardin D, a Natural Product Derived from Liverwort Plant Dumortiera hirsuta

Inhibitory effect of riccardin D on growth of human non-small cell lung cancer: In vitro and in vivo studies

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Gonadotropin-releasing hormone-agonist induces apoptosis of human granulosa-luteal cells <i>via</i> caspase-8, -9 and -3, and poly-(ADP-ribose)-polymerase cleavage

Cited by 23 publications

References 44 publications

Chemoprevention of intestinal adenomatous polyposis by acetyl‐11‐keto‐beta‐boswellic acid in APCMin/+ mice

Chemoprevention of intestinal adenomatous polyposis by acetyl‐11‐keto‐beta‐boswellic acid in APCMin/+ mice

Inhibition of Intestinal Adenoma Formation in APCMin/+ Mice by Riccardin D, a Natural Product Derived from Liverwort Plant Dumortiera hirsuta

Inhibitory effect of riccardin D on growth of human non-small cell lung cancer: In vitro and in vivo studies

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Chemoprevention of intestinal adenomatous polyposis by acetyl‐11‐keto‐beta‐boswellic acid in APC^Min/+ mice

Chemoprevention of intestinal adenomatous polyposis by acetyl‐11‐keto‐beta‐boswellic acid in APC^Min/+ mice