Cancer Research and Treatment

Original Articles

Anti-cancer Effects of a Novel Quinoline Derivative 83b1 on Human Esophageal Squamous Cell Carcinoma through Down-Regulation of COX-2 mRNA and PGE₂: Ivan Ho Yuen Pun, Dessy Chan, Sau Hing Chan, Po Yee Chung, Yuan Yuan Zhou, Simon Law, Alfred King Yin Lam, Chung Hin Chui, Albert Sun Chi Chan, Kim Hung Lam, Johnny Cheuk On Tang; Cancer Res Treat. 2017;49(1):219-229. Published online July 18, 2016; DOI: https://doi.org/10.4143/crt.2016.190

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Purpose
83b1 is a novel quinoline derivative that has been shown to inhibit cancer growth in human esophageal squamous cell carcinoma (ESCC). This study was conducted to comprehensively evaluate the cytotoxic effects of 83b1 on a series of ESCC cell lines and investigate the mechanisms by which 83b1 suppresses cancer growth based on molecular docking analysis.
Materials and Methods
A series of ESCC and nontumor immortalized cell lines were exposed to 83b1 and cisplatin (CDDP) in a dose-dependent manner, and the cytotoxicity was examined by a MTS assay kit. Prediction of the molecular targets of 83b1 was conducted by molecular docking analysis. Expression of cyclooxygenase 2 (COX-2) mRNA and COX-2–derived prostaglandin E2 (PGE2) were measured by quantitative real-time polymerase chain reaction and enzymelinked immuno-sorbent assay, respectively. In vivo anti-tumor effect was determined using a nude mice xenografted model transplanted with an ESCC cell line, KYSE-450.
Results
83b1 showed the significant anti-cancer effects on all ESCC cell lines compared to CDDP; however, 83b1 revealed much lower toxic effects on non-tumor cell lines than CDDP. The predicted molecular target of 83b1 is peroxisome proliferator-activated receptor delta (PPARδ), which is a widely known oncoprotein. Additionally the expression of COX-2 mRNA and COX-2–derived PGE2 were down-regulated by 83b1 in a dose-dependent manner in ESCC cell lines. Furthermore, 83b1 was shown to significantly reduce the tumor size in nude mice xenograft.
Conclusion
The results of this study suggest that the potential anti-cancer effects of 83b1 on human esophageal cancers occur through the possible oncotarget, PPARδ, and down-regulation of the cancer related genes and molecules.

Citations

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Microwave‐Promoted Multicomponent Synthesis Catalyzed by DABCO, Anti‐Esophageal Cancer, Apoptotic Morphology, Kinetic Mechanism, and Computational Studies of New Pyrrole Derivatives
Ahmed Majeed Jassem, Bahjat A. Saeed
ChemistrySelect.2026;[Epub] CrossRef
Arachidonic acid metabolism as a novel pathogenic factor in gastrointestinal cancers
Weiqin Lu, Aihemaitijiang Aihaiti, Paziliya Abudukeranmu, Yajun Liu, Huihui Gao
Molecular and Cellular Biochemistry.2025; 480(2): 1225. CrossRef
Synthesis and biological evaluation of novel 2-morpholino-4-anilinoquinoline derivatives as antitumor agents against HepG2 cell line
Ahmed Al-Sheikh, Malak A. Jaber, Hana'a Khalaf, Nour AlKhawaja, Duaa Abuarqoub
RSC Advances.2024; 14(5): 3304. CrossRef
Natural alkaloids as potential treatments for esophageal squamous-cell carcinoma: A comprehensive review
Eugene Jamot Ndebia, Gabriel Tchuente Kamsu
Gastroenterology & Endoscopy.2024; 2(3): 131. CrossRef
Downregulation of chemokine (C‑C motif) ligand 5 induced by a novel 8‑hydroxyquinoline derivative (91b1) suppresses tumor invasiveness in esophageal carcinoma
Johnny Tang, Dessy Chan, Po-Yee Chung, Yijiang Liu, Alfred Lam, Simon Law, Wolin Huang, Albert Chan, Kim-Hung Lam, Yuanyuan Zhou
International Journal of Molecular Medicine.2024;[Epub] CrossRef
Peroxisome proliferator-activated receptors regulate the progression and treatment of gastrointestinal cancers
Min Zhang, Shujie He
Frontiers in Pharmacology.2023;[Epub] CrossRef
Roles of Nuclear Receptors in Esophageal Cancer
Lihao Deng, Jiaxuan Liu, Wei-Dong Chen, Yan-Dong Wang
Current Pharmaceutical Biotechnology.2023; 24(12): 1489. CrossRef
Synthesis and biological activities of new phthalimide and thiazolidine derivatives
Flaviana A. Santos, Marcel L. Almeida, Vitor A. S. Silva, Douglas C. F. Viana, Michelly C. Pereira, André S. L. Lucena, Maira G. R. Pitta, Marina R. Galdino-Pitta, Moacyr J. B. de Melo Rêgo, Ivan da Rocha Pitta
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Cancer Prevention Research.2022; 15(6): 355. CrossRef
The Anticancer Effect of a Novel Quinoline Derivative 91b1 through Downregulation of Lumican
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Synthesis and biological evaluations of N′-substituted methylene-4-(quinoline-4-amino) benzoylhydrazides as potential anti-hepatoma agents
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Bioorganic Chemistry.2020; 96: 103592. CrossRef
Feasibility of Repurposing Clioquinol for Cancer Therapy
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Recent Patents on Anti-Cancer Drug Discovery.2020; 15(1): 14. CrossRef
DFIQ, a Novel Quinoline Derivative, Shows Anticancer Potential by Inducing Apoptosis and Autophagy in NSCLC Cell and In Vivo Zebrafish Xenograft Models
Hurng-Wern Huang, Yung-Ding Bow, Chia-Yih Wang, Yen-Chun Chen, Pei-Rong Fu, Kuo-Feng Chang, Tso-Wen Wang, Chih-Hua Tseng, Yeh-Long Chen, Chien-Chih Chiu
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Reverse Screening Methods to Search for the Protein Targets of Chemopreventive Compounds
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The roles of the COX2/PGE2/EP axis in therapeutic resistance
Dali Tong, Qiuli Liu, Lin-ang Wang, Qiubo Xie, Jian Pang, Yiqiang Huang, Luofu Wang, Gaolei Liu, Dianzheng Zhang, Weihua Lan, Jun Jiang
Cancer and Metastasis Reviews.2018; 37(2-3): 355. CrossRef
Expression of Insulin-Like Growth Factor Binding Protein-5 (IGFBP5) Reverses Cisplatin-Resistance in Esophageal Carcinoma
Dessy Chan, Yuanyuan Zhou, Chung Hin Chui, Kim Hung Lam, Simon Law, Albert Sun-chi Chan, Xingshu Li, Alfred King-yin Lam, Johnny Cheuk On Tang
Cells.2018; 7(10): 143. CrossRef
Targeting DNA Binding for NF-κB as an Anticancer Approach in Hepatocellular Carcinoma
Po Chung, Pik Lam, Yuanyuan Zhou, Jessica Gasparello, Alessia Finotti, Adriana Chilin, Giovanni Marzaro, Roberto Gambari, Zhaoxiang Bian, Wai Kwok, Wai Wong, Xi Wang, Alfred Lam, Albert Chan, Xingshu Li, Jessica Ma, Chung Chui, Kim Lam, Johnny Tang
Cells.2018; 7(10): 177. CrossRef

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TGF-β Suppresses COX-2 Expression by Tristetraprolin-Mediated RNA Destabilization in A549 Human Lung Cancer Cells: Soyeong Kang, Ahrum Min, Seock-Ah Im, Sang-Hyun Song, Sang Gyun Kim, Hyun-Ah Kim, Hee-Jun Kim, Do-Youn Oh, Hyun-Soon Jong, Tae-You Kim, Yung-Jue Bang; Cancer Res Treat. 2015;47(1):101-109. Published online October 22, 2014; DOI: https://doi.org/10.4143/crt.2013.192

Abstract PDF PubReader ePub

Purpose
Overexpression of cyclooxygenase 2 (COX-2) is thought to promote survival of transformed cells. Transforming growth factor β (TGF-β) exerts anti-proliferative effects on a broad range of epithelial cells. In the current study, we investigated whether TGF-β can regulate COX-2 expression in A549 human lung adenocarcinoma cells, which are TGF-β-responsive and overexpress COX-2.
Materials and Methods
Western blotting, Northern blotting, and mRNA stability assays were performed to demonstrate that COX-2 protein and mRNA expression were suppressed by TGF-β. We also evaluated the effects of tristetraprolin (TTP) on COX-2 mRNA using RNA interference.
Results
We demonstrated that COX-2 mRNA and protein expression were both significantly suppressed by TGF-β. An actinomycin D chase experiment demonstrated that COX-2 mRNA was more rapidly degraded in the presence of TGF-β, suggesting that TGF-β–induced inhibition of COX-2 expression is achieved via decreased mRNA stability. We also found that TGF-β rapidly and transiently induced the expression of TTP, a well-known mRNA destabilizing factor, before suppression of COX-2 mRNA expression was observed. Using RNA interference, we confirmed that increased TTP levels play a pivotal role in the destabilization of COX-2 mRNA by TGF-β. Furthermore, we showed that Smad3 is essential to TTP-dependent down-regulation of COX-2 expression in response to TGF-β.
Conclusion
The results of this study show that TGF-β down-regulated COX-2 expression via mRNA destabilization mediated by Smad3/TTP in A549 cells.

Citations

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Yanli Wang, Yiyao Gong, Muhammad Salman Farid, Changhui Zhao
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Tristetraprolin, a Potential Safeguard Against Carcinoma: Role in the Tumor Microenvironment
Diwen Zhang, Zhigang Zhou, Ruixia Yang, Sujun Zhang, Bin Zhang, Yanxuan Tan, Lingyao Chen, Tao Li, Jian Tu
Frontiers in Oncology.2021;[Epub] CrossRef
Pan-Pim Kinase Inhibitor AZD1208 Suppresses Tumor Growth and Synergistically Interacts with Akt Inhibition in Gastric Cancer Cells
Miso Lee, Kyung-Hun Lee, Ahrum Min, Jeongeun Kim, Seongyeong Kim, Hyemin Jang, Jee Min Lim, So Hyeon Kim, Dong-Hyeon Ha, Won Jae Jeong, Koung Jin Suh, Yae-Won Yang, Tae Yong Kim, Do-Youn Oh, Yung-Jue Bang, Seock-Ah Im
Cancer Research and Treatment.2019; 51(2): 451. CrossRef
Transforming Growth Factor β Activation Primes Canonical Wnt Signaling Through Down‐Regulation of Axin‐2
Justin Gillespie, Rebecca L. Ross, Clarissa Corinaldesi, Filomena Esteves, Emma Derrett‐Smith, Michael F. McDermott, Gina M. Doody, Christopher P. Denton, Paul Emery, Francesco Del Galdo
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Cyclin E overexpression confers resistance to the CDK4/6 specific inhibitor palbociclib in gastric cancer cells
Ahrum Min, Jung Eun Kim, Yu-Jin Kim, Jee Min Lim, Seongyeong Kim, Jin Won Kim, Kyung-Hun Lee, Tae-Yong Kim, Do-Youn Oh, Yung-Jue Bang, Seock-Ah Im
Cancer Letters.2018; 430: 123. CrossRef
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Martha Lappas
Mediators of Inflammation.2018; 2018: 1. CrossRef
Tristetraprolin activation by resveratrol inhibits the proliferation and metastasis of colorectal cancer cells
Se-Ra Lee, Hua Jin, Won-Tae Kim, Won-Jung Kim, Sung Zoo Kim, Sun-Hee Leem, Soo Mi Kim
International Journal of Oncology.2018;[Epub] CrossRef
Androgen Receptor Inhibitor Enhances the Antitumor Effect of PARP Inhibitor in Breast Cancer Cells by Modulating DNA Damage Response
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Molecular Cancer Therapeutics.2018; 17(12): 2507. CrossRef
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Antitumor Effect of KX-01 through Inhibiting Src Family Kinases and Mitosis
Seongyeong Kim, Ahrum Min, Kyung-Hun Lee, Yaewon Yang, Tae-Yong Kim, Jee Min Lim, So Jung Park, Hyun-Jin Nam, Jung Eun Kim, Sang-Hyun Song, Sae-Won Han, Do-Youn Oh, Jee Hyun Kim, Tae-You Kim, David Hangauer, Johnson Yiu-Nam Lau, Kyongok Im, Dong Soon Lee,
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Ahrum Min, Seock-Ah Im, Hyemin Jang, Seongyeong Kim, Miso Lee, Debora Keunyoung Kim, Yaewon Yang, Hee-Jun Kim, Kyung-Hun Lee, Jin Won Kim, Tae-Yong Kim, Do-Youn Oh, Jeff Brown, Alan Lau, Mark J. O'Connor, Yung-Jue Bang
Molecular Cancer Therapeutics.2017; 16(4): 566. CrossRef
HSP90 Inhibition Suppresses PGE2 Production via Modulating COX-2 and 15-PGDH Expression in HT-29 Colorectal Cancer Cells
A. Mohammadi, M.M. Yaghoobi, A. Gholamhoseinian Najar, B. Kalantari-Khandani, H. Sharifi, M. Saravani
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Dysregulation of TTP and HuR plays an important role in cancers
Hao Wang, Nannan Ding, Jian Guo, Jiazeng Xia, Yulan Ruan
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Low tristetraprolin expression promotes cell proliferation and predicts poor patients outcome in pancreatic cancer
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Pattern of Apoptosis by NS398, a Selective COX-2 Inhibitor, in Hepatocellular Carcinoma Cell Lines: Mi Kyung Park, Moon Kyu Kim, Jung Chul Kim, Young Kwan Sung; Cancer Res Treat. 2005;37(5):313-317. Published online October 31, 2005; DOI: https://doi.org/10.4143/crt.2005.37.5.313

Abstract PDF PubReader ePub

Purpose

NS398, a selective COX-2 inhibitor, is known to inhibit the growth of COX-2 expressing hepatocellular carcinoma cells. The present study investigated whether the cytotoxic effect of NS398 was COX-2 dependent and whether caspases were involved in NS398-induced apoptosis in hepatocellular carcinoma cells.

Materials and Methods

The expressions of COX-2 in SNU 423 and SNU 449 hepatocellular carcinoma cell lines were examined using RT-PCR and Western blot. The cytotoxic effect of NS398 was measured using MTT in the presence or absence of caspase inhibitors. The distribution of the cell cycle and extent of apoptosis were analyzed using flow cytometry and a Cell Death Elisa kit, respectively.

Results

The expression of COX-2 was observed in SNU423 cells, but not in SNU 449 cells. NS398 treatment resulted in both dose-and time-dependent growth inhibitions, with increases in apoptotic cells in both cell lines. Treatment with the pan-caspase inhibitor, z-VAD- fmk, or the caspase-3 inhibitor, Ac-DMQD-CHO, showed no attenuation of the cytotoxic effect of NS398 in either cell line.

Conclusion

This study demonstrated that the cytotoxic effect of NS398 was independent of COX-2 expression. Caspases were also shown not to be involved in NS398-induced apoptosis in either SNU 423 or SNU 449 Korean HCC cell lines. Our data suggests the feasibility of preventing hepatocellular carcinoma with the use of COX-2 inhibitors needs to be carefully evaluated.

Citations

Citations to this article as recorded by

First study on the immunohistochemical expression of cyclooxygenase-2 and clinicopathological association in canine hepatoid gland neoplasms
Pinkarn Chantawong, Thanongsak Mamom, Sahatchai Tangtrongsup, Setthakit Chitsanoor, Hassadin Boonsriroj
Veterinary World.2022; : 2432. CrossRef
Evaluation of Cytotoxicity Effects of Chalcone Epoxide Analogues as a Selective COX-II Inhibitor in the Human Liver Carcinoma Cell Line
Bahram Daraei, Gholamreza Karimi, Pouran Makhdoumi, Afshin Zarghi
Journal of Pharmacopuncture.2017; 20(3): 207. CrossRef
RETRACTED ARTICLE: Effect of NS-398, a cyclooxygenase-2 selective inhibitor, on the cytotoxicity of cytotoxic T lymphocytes to ovarian carcinoma cells
Xinyan Wang, Yu Liang, Jun Wang, Min Wang
Tumor Biology.2013; 34(3): 1517. CrossRef
Gene Expression Profile of Coronary Artery Cells Treated With Nonsteroidal Anti-inflammatory Drugs Reveals Off-target Effects
Sanjeewani T. Palayoor, Molykutty J-Aryankalayil, Adeola Y. Makinde, David Cerna, Michael T. Falduto, Scott R. Magnuson, C. Norman Coleman
Journal of Cardiovascular Pharmacology.2012; 59(6): 487. CrossRef

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Co-Expression of Cox-2, C-Met and β-catenin in Cells Forming Invasive front of Gallbladder Cancer: Woo Sung Moon, Ho Sung Park, Ho Lee, Rama Pai, Andrzej S. Tarnawski, Kyung Ryoul Kim, Kyu Yun Jang; Cancer Res Treat. 2005;37(3):171-176. Published online June 30, 2005; DOI: https://doi.org/10.4143/crt.2005.37.3.171

Abstract PDF PubReader ePub

Purpose

Gallbladder cancer is a malignancy with poor prognosis, predominantly resulting from invasion and metastasis. Our previous studies have demonstrated that prostaglandin E₂ (PGE₂), generated by cyclooxygenase 2 (Cox-2), transactivates epidermal growth factor receptor (EGFR), c-Met and β-catenin; thus, enhancing colon cancer cell growth and invasiveness in vitro. To determine whether these findings are applicable to clinical conditions, we examined the expression and cellular localization/co-localization of Cox-2, c-Met, β-catenin, EGFR and c-erbB2 in gallbladder cancer.

Materials and Methods

Thirty-five specimens of invasive gallbladder cancer, 8 in situ carcinoma and 7 adenoma specimens were immunostained with specific antibodies against Cox-2, c-Met, β-catenin, EGFR and c-erbB2. The cellular distribution, localization and colocalization were examined, and the signal intensities quantified in: a) the central area of gallbladder cancer and b) cancer cells forming the invasive front.

Results

Cox-2, c-Met, β-catenin, c-erbB2 and EGFR were over-expressed in 80, 74, 71, 62 and 11% of invasive gallbladder cancers, respectively. β-catenin was expressed in 80% of non-malignant specimens, exclusively in the cell membrane, while the cancer specimens showed cytoplasmic and/or nuclear staining. Significantly higher Cox-2, c-Met and β-catenin expressions were present in cancer cells of the invasive front than in the tumor central areas (p<0.001), and these expressions were significantly (p=0.01) associated with the invasion depth. Co-expressions of Cox-2, c-Met, β-catenin and c-erbB2 were present in 42% of the specimens in cancer cells forming the invasive front.

Conclusion

The overexpressions, and often co-localizations, of Cox-2, c-Met and β-catenin in cancer cells forming the invasive front indicate their local interactions and important roles in invasion.

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