Cancer Research and Treatment

Original Articles

Effect of Estradiol in an Azoxymethane/Dextran Sulfate Sodium-Treated Mouse Model of Colorectal Cancer: Implication for Sex Difference in Colorectal Cancer Development: Hee Jin Son, Sung Hwa Sohn, Nayoung Kim, Ha-Na Lee, Sun Min Lee, Ryoung Hee Nam, Ji Hyun Park, Chin-Hee Song, Eun Shin, Hee Young Na, Joo Sung Kim, Dong Ho Lee, Young-Joon Surh; Cancer Res Treat. 2019;51(2):632-648. Published online August 1, 2018; DOI: https://doi.org/10.4143/crt.2018.060

Abstract PDF Supplementary Material PubReader ePub

Purpose
This study demonstrates that estradiol downregulates inflammation and inhibits colorectal cancer (CRC) development in azoxymethane/dextran sulfate sodium (AOM/DSS) mouse model.
Materials and Methods
AOM/DSS-treated male and female mice were sacrificed at weeks 2, 10, and 16, to assess estrogen effects on colitis and carcinogenesis. Macroscopic and histologic severity of colitis and Western blot and quantitative real-time polymerase chain reaction were evaluated, to measure inflammatory mediators and cytokines.
Results
Compared with AOM/DSS-treated male mice (M-AOM/DSS group), AOM/DSS-treated male mice with estradiol administration (M-AOM/DSS+estr group) displayed at week 2 significantly decreased severity of colitis. At weeks 10 and 16, AOM/DSS-treated female mice (F-AOM/DSS group) and the M-AOM/DSS+estr group showed significantly lower tumor multiplicity compared with the M-AOM/DSS group. At week 2, F-AOM/DSS group had a lower level of nuclear factor-κB (NF-κB) expression and higher level of nuclear factor erythroid 2-related factor 2 (Nrf2) expression, compared to the M-AOM/DSS group. At week 2, expression levels of NF-κB and its related mediators decreased in the M-AOM/DSS+estr group, while levels of Nrf2 and Nrf2-related anti-oxidant enzymes increased. In addition, estradiol significantly increased Nod-like receptor protein 3 (NLRP3) inflammasome expressions in AOM/DSS-treated male mice. In contrast, at weeks 10 and 16, Nrf2 and its-related anti-oxidant enzymes and NLRP3 inflammasome were highly expressed in M-AOM/DSS group and in F-AOM/DSS group, who developed cancer.
Conclusion
The data suggest that estradiol inhibits the initiation of CRC by regulating Nrf2-related pathways. Moreover, these imply the dual role of Nrf2 and NLRP3 inflammasome, including promotion of tumor progression upon tumor initiation.

Citations

Citations to this article as recorded by

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Synergistic Effect of COX-2 Inhibitor on Paclitaxel-Induced Apoptosis in the Human Ovarian Cancer Cell Line OVCAR-3: Hee Jung Kim, Ga Won Yim, Eun Ji Nam, Young Tae Kim; Cancer Res Treat. 2014;46(1):81-92. Published online January 15, 2014; DOI: https://doi.org/10.4143/crt.2014.46.1.81

Abstract PDF PubReader ePub

PURPOSE
Celecoxib, a highly selective cyclooxygenase-2 inhibitor, regulates apoptosis of several types of human cancer cells. The purpose of this study was to investigate whether celecoxib in combination with paclitaxel modulates apoptosis of ovarian cancer cells, and to identify the signal pathway by which celecoxib mediates apoptosis.
MATERIALS AND METHODS
OVCAR-3 cells were exposed to paclitaxel (20 microM) in the absence or presence of celecoxib (10 microM). Cell viability was evaluated using a Cell Counting Kit-8 assay. Apoptosis was evaluated using Annexin-V/7-aminoactinomycin D staining and a cellular DNA fragmentation enzyme-linked immunosorbent assay. Caspase-3, -9, and cleavage of poly ADP-ribose polymerase (PARP) were determined by western blotting. Expression of nuclear factor-kappaB (NF-kappaB) and vascular endothelial growth factor (VEGF) and Akt activation were assessed using reverse transcriptase-polymerase chain reaction and western blotting.
RESULTS
Celecoxib enhanced paclitaxel-induced growth inhibition of OVCAR-3 cells. Celecoxib significantly increased paclitaxel-induced apoptosis of OVCAR-3 cells. Pretreatment with celecoxib also increased activation of caspase-9, -3 and cleaved PARP following paclitaxel-treatment. Exposure of OVCAR-3 cells to celecoxib in combination with paclitaxel resulted in downregulation of NF-kappaB activation and VEGF expression. Furthermore, combining celecoxib and paclitaxel inhibited phosphorylation of Akt.
CONCLUSION
OVCAR-3 cells were sensitized to paclitaxel-induced apoptosis by celecoxib through downregulation of NF-kappaB and Akt activation, suggesting that celecoxib may work synergistically with paclitaxel to inhibit different targets and ultimately produce anticancer effects. Combining celecoxib with paclitaxel may prove beneficial in the clinical treatment of ovarian cancer.

Citations

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Journal of Taibah University for Science.2023;[Epub] CrossRef
Celecoxib Reverse Invasion and Metastasis of Gastric Cancer through Lnc_AC006548.28-miR-223-LAMC2 Pathway
Guohua Jin, Jianguang Zhang, Tingting Cao, He Zhu, Yang Shi, Kapil Sharma
Computational Intelligence and Neuroscience.2022; 2022: 1. CrossRef
New Visions on Natural Products and Cancer Therapy: Autophagy and Related Regulatory Pathways
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Indian Journal of Surgery.2021; 83(4): 932. CrossRef
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Mohammad Panji, Vahideh Behmard, Zahra Zare, Monireh Malekpour, Hasan Nejadbiglari, Saeede Yavari, Tina Nayerpour dizaj, Azadeh Safaeian, Ali Bakhshi, Omid Abazari, Mojtaba Abbasi, Parisa Khanicheragh, Maryam Shabanzadeh
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Lin Deng, Ding-qing Feng, Bin Ling
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Di Yu‐Wei, Zhuo‐sheng Li, Shu‐min Xiong, Ge Huang, Yan‐fei Luo, Tie‐ying Huo, Mao‐hua Zhou, You‐wei Zheng
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Zhuyan Shao, Qiang Wen, Tao Zhu, Wei Jiang, Yu Kang, Conjian Xu, Shihua Wang
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The Chemopreventive Effect of Retinoids on Cellular NF-κB Activity Induced by NMU and NEU in Human Malignant Keratinocytes: Ki-Young Moon; Cancer Res Treat. 2007;39(2):82-87. Published online June 30, 2007; DOI: https://doi.org/10.4143/crt.2007.39.2.82

Abstract PDF PubReader ePub

Purpose

Retinoids have been shown to be effective in suppressing tumor development when chemical carcinogens such as N-nitroso-N-methylurea (NMU) and N-nitroso-N-ethylurea (NEU) were used to induce mammary tumors in a variety of animal models. However, the molecular mechanisms associated with the retinoid-mediated chemopreventive process, as linked to transcription factor NF-κB activation, for chemoprevention have not been elucidated. The purpose of this study was to determine the implications of NF-κB activation on the chemopreventive role of retinoids and their effect on cellular NF-κB activity that's induced by known alkylating chemical carcinogens such as NMU and NEU in human transfectant squamous cell carcinoma (SCC-13) cells.

Materials and Methods

The activity of NF-κB, as regulated by chemical carcinogens and retinoids, was determined in cultured human SCC-13 keratinocytes that were transfected with the pNF-κB-SEAP-NPT plasmid; this permitted the expression of the secretory alkaline phosphatase (SEAP) reporter gene in response to the NF-κB activity, and the plasmid contained the neomycin phosphotransferase (NPT) gene, which confers resistance to geneticin. The reporter enzyme activity was measured using a fluorescence detection assay method.

Results

All-trans retinoic acid and 13-cis retinoic acid induced a reduction of NF-κB activity up to 64% and 65%, respectively, compared to the control. For the treatment of the human transfectant cells with chemical carcinogens, all-trans retinoic acid (5 mM) and 13-cis retinoic acid (5 mM) downregulated the cellular NF-κB activation up to 83% and 85% compared to the NF-κB activity that was upregulated by NMU (5µM) and NEU (5µM), respectively.

Conclusion

These results suggest that the chemopreventive effect of retinoids may be mediated by the downregulated activation of NF-κB and that retinoids are implicated in the activation of NF-κB in human skin cells.

Citations

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Upregulation of Nitric Oxide Synthase Activity by All-transRetinoic Acid and 13-cisRetinoic Acid in Human Malignant Keratinocytes
Ki-Young Moon
Biomedical Science Letters.2019; 25(2): 196. CrossRef
N-nitroso-N-methylurea and N-nitroso-N-ethylurea Decrease in Nitric Oxide Production in Human Malignant Keratinocytes
Ki-Young Moon
Biomedical Science Letters.2018; 24(1): 50. CrossRef
Inhibitory Effect of Retinoids on Alkaline Phosphatase Isoenzymes Activity in Human Serum
Seung Hee Kim, Ki-Young Moon
Biomedical Science Letters.2017; 23(3): 230. CrossRef
Targeting Neuroblastoma Stem Cells with Retinoic Acid and Proteasome Inhibitor
Barbara Hämmerle, Yania Yañez, Sarai Palanca, Adela Cañete, Deborah J. Burks, Victoria Castel, Jaime Font de Mora, Yiqun G. Shellman
PLoS ONE.2013; 8(10): e76761. CrossRef
Retinoids: novel immunomodulators and tumour‐suppressive agents?
MR Carratù, C Marasco, G Mangialardi, A Vacca
British Journal of Pharmacology.2012; 167(3): 483. CrossRef
Acrolein, an I-κBα-independent downregulator of NF-κB activity, causes the decrease in nitric oxide production in human malignant keratinocytes
Ki-Young Moon
Archives of Toxicology.2011; 85(5): 499. CrossRef
N-nitroso-N-methylurea and N-nitroso-N-ethylurea induce upregulation of cellular NF-κ B activity through protein kinase C-dependent pathway in human malignant keratinocytes
Ki-Young Moon
Archives of Pharmacal Research.2010; 33(1): 133. CrossRef

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