Cancer Research and Treatment

Original Articles

Prognostic Impact of Polymorphisms in the CASPASE Genes on Survival of Patients with Colorectal Cancer: Jun Young Choi, Jong Gwang Kim, You Jin Lee, Yee Soo Chae, Sang Kyun Sohn, Joon Ho Moon, Byung Woog Kang, Min Kyu Jung, Seong Woo Jeon, Jun Seok Park, Gyu Seog Choi; Cancer Res Treat. 2012;44(1):32-36. Published online March 31, 2012; DOI: https://doi.org/10.4143/crt.2012.44.1.32

PURPOSE
This study analyzed potentially functional polymorphisms in CASPASE (CASP) genes and their impact on the prognosis for Korean colorectal cancer patients.
MATERIALS AND METHODS
A total of 397 consecutive patients with curatively resected colorectal adenocarcinoma were enrolled in this study. Genomic DNA from these patients was extracted from fresh colorectal tissue, and the 10 polymorphisms in the CASP3, CASP6, CASP7, CASP8, CASP9, and CASP10 genes were determined using a reverse transcription polymerase chain reaction genotyping assay.
RESULTS
The median patient age was 63 years, and 218 (54.9%) patients had colon cancer, while 179 (45.1%) patients had rectal cancer. Univariate and multivariate survival analysis including pathologic stage, patient age, differentiation, and carcinoembryonic antigen level demonstrated that these polymorphisms were not associated with either disease-free or overall survival.
CONCLUSION
None of the 10 polymorphisms in the CASP genes investigated in this study was found to be an independent prognostic marker for Korean patients with curatively resected colorectal cancer.

Citations

Citations to this article as recorded by

Immune-related gene-based model predicts the survival of colorectal carcinoma and reflected various biological statuses
Zhengchun Kang, Bingchen Chen, Xiuzhu Ma, Feihu Yan, Zhen Wang
Frontiers in Molecular Biosciences.2023;[Epub] CrossRef
TCGA dataset screening for genes implicated in endometrial cancer using RNA-seq profiling
Xiaoli Fu, Shuai Cheng, Wei Wang, Oumin Shi, Fuxiao Gao, Yong Li, Qi Wang
Cancer Genetics.2021; 254-255: 40. CrossRef
Mutational analysis of apoptotic genes in familial aggregation of hematological malignancies
Walid Sabri Hamadou, Rahma Mani, Nouha Bouali, Sawsen Besbes, Violaine Bourdon, Rym El Abed, Yosra Ben Youssef, Véronique Mari, Paul Gesta, Hélène Dreyfus, Valérie Bonadona, Catherine Dugast, Hélène Zattara, Laurence Faivre, Tetsuro Noguchi, Abderrahim Kh
Bulletin du Cancer.2021; 108(9): 798. CrossRef
Construction and Characterization of a Synergistic lncRNA–miRNA Network Reveals a Crucial and Prognostic Role of lncRNAs in Colon Cancer
Bin Zhao, Xiusheng Qu, Xin Lv, Qingdong Wang, Deqiang Bian, Fan Yang, Xingwang Zhao, Zhiwu Ji, Jian Ni, Yan Fu, Guorong Xin, Haitao Yu
Frontiers in Genetics.2020;[Epub] CrossRef
CASP8 (rs3834129) and CASP3 (rs4647601) polymorphisms in oropharynx cancer risk, tumor cell differentiation, and prognosis in a cohort of the Brazilian population
Gabriela Arielo Tortorelli, Caroline Torricelli, Juliana Carron, Ericka Francislaine Dias Costa, Leisa Lopes-Aguiar, Bruna Fernandes Carvalho, José Augusto Rinck-Junior, Fernanda Viviane Mariano, Albina Messias Almeida Milani Altemani, Carmen Silvia Passo
Molecular Biology Reports.2019; 46(6): 6557. CrossRef
Screening for implicated genes in colorectal cancer using whole‑genome gene expression profiling
Long‑Ci Sun, Hai‑Xin Qian
Molecular Medicine Reports.2018;[Epub] CrossRef
Apoptosis-inducing and antiproliferative effect by inhibition of miR-182-5p through the regulation of CASP9 expression in human breast cancer
M Sharifi, A Moridnia
Cancer Gene Therapy.2017; 24(2): 75. CrossRef
Inducing cell proliferative prevention in human acute promyelocytic leukemia by miR-182 inhibition through modulation of CASP9 expression
Mahdi Fasihi-Ramandi, Abbas Moridnia, Ali Najafi, Mohammadreza Sharifi
Biomedicine & Pharmacotherapy.2017; 89: 1152. CrossRef
Genetic variants in cell death pathway genes and HBV-related hepatocellular carcinoma among a Chinese Han population
Fei Liu, Fuqiang Li, Limei Luo, Hanteng Yang, Yonggang Wei, Wentao Wang, Lvnan Yan, Tianfu Wen, Jiayin Yang, Bo Li
Apoptosis.2017; 22(8): 1035. CrossRef
Associations of genetic variation in CASP3 gene with noise-induced hearing loss in a Chinese population: a case–control study
Yinyin Wu, Juntao Ni, Mingjian Qi, Chengjian Cao, Yuxian Shao, Liangwen Xu, Haiyan Ma, Lei Yang
Environmental Health.2017;[Epub] CrossRef
CASP8-652 6N insertion/deletion polymorphism and overall cancer risk: evidence from 49 studies
Jiarong Cai, Qingjian Ye, Suling Luo, Ze Zhuang, Kui He, Zhen-Jian Zhuo, Xiaochun Wan, Juan Cheng
Oncotarget.2017; 8(34): 56780. CrossRef
Association between main Caspase Gene Polymorphisms and the Susceptibility and Prognosis of Colorectal Cancer
Zhiwei Wu, Ye Li, Shuying Li, Lin Zhu, Guangxiao Li, Zhifu Yu, Xiaojuan Zhao, Jie Ge, Binbin Cui, Xinshu Dong, Suli Tian, Fulan Hu, Yashuang Zhao
Medical Oncology.2013;[Epub] CrossRef

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Resveratrol at High Doses Acts as an Apoptotic Inducer in Endothelial Cells: Kyungmin In, Jongbong Park, Heonyong Park; Cancer Res Treat. 2006;38(1):48-53. Published online February 28, 2006; DOI: https://doi.org/10.4143/crt.2006.38.1.48

Abstract PDF PubReader ePub

Purposes

Resveratrol is a phenolic compound found in grapes and other food products. In order to assess the availability of resveratrol as an angio-inhibiting drug, we examined whether resveratrol plays an important role in bovine aortic endothelial cells (BAECs) for cell apoptosis and cell migration.

Methods and Materials

Endothelial cell apoptosis was observed as detected by the Hoechst staining and the caspase-3 activity. Additionally, Western blotting was performed for monitoring the activities of various cell signaling molecules.

Results

Resveratrol was shown to act as a pro-apoptotic agent. The pro-apoptotic effect of resveratrol was as great as that of etoposide, a well-known anti-cancer drug. In addition, resveratrol had an inhibitory effect on endothelial cell migration. The demonstrated efficacy of resveratrol suggests that resveratrol may be utilized as an anti-angiogenic drug. To determine the underlying mechanisms, we further investigated which signaling molecules are activated by resveratrol. Extracellular signal-regulated kinase (ERK) was activated by the treatment with resveratrol in BAECs, whereas endothelial nitric oxide synthetase (eNOS), Akt, and Jun N-terminal kinase (JNK) were inhibited. The pretreatment with PD compound, an ERK inhibitor, had no effect on the pro-apoptosis induced by resveratrol.

Conclusion

Resveratrol plays an important role in endothelial cell apoptosis, indicating that resveratrol can be utilized as a potent anti-angiogenic drug.

Citations

Citations to this article as recorded by

Novel plasma-polymerized coating facilitates HeLa cell spheroid formation, exerting necroptosis via β-cyclodextrin-encapsulated resveratrol
Sujeong Jang, Namwuk Baek, Youngsik Seo, Hyuna Lim, Donggeun Jung, Heonyong Park
Journal of Analytical Science and Technology.2024;[Epub] CrossRef
Effect of eIF2α in Neuronal Injury Induced by High Glucose and the Protective Mechanism of Resveratrol
Lijing Zhang, Kaining Zhi, Yanfang Su, Wenpeng Peng, Xianfang Meng
Molecular Neurobiology.2023; 60(10): 6043. CrossRef
A comparison of resveratrol and other polyphenolic compounds on Notch activation and endothelial cell activity
Bryce LaFoya, Jordan A. Munroe, Allan R. Albig, Myon-Hee Lee
PLOS ONE.2019; 14(1): e0210607. CrossRef
Resveratrol-Induced Temporal Variation in the Mechanical Properties of MCF-7 Breast Cancer Cells Investigated by Atomic Force Microscopy
Jagoba Iturri, Andreas Weber, Alberto Moreno-Cencerrado, Maria dM Vivanco, Rafael Benítez, Stefano Leporatti, José Luis Toca-Herrera
International Journal of Molecular Sciences.2019; 20(13): 3275. CrossRef
Effect of Fermented Platycodon grandiflorum Extract on Cell Proliferation and Migration in Bovine Aortic Endothelial Cells
Woosoung Choi, Jina Song, Mi-Hyeon Park, Heui Jong Yu, Heonyong Park
Journal of Life Science.2016; 26(1): 59. CrossRef
Resveratrol inhibits cell cycle progression by targeting Aurora kinase A and Polo-like kinase 1 in breast cancer cells
RUBICELI MEDINA-AGUILAR, LAURENCE A. MARCHAT, ELENA ARECHAGA OCAMPO, PATRICIO GARIGLIO, JAIME GARCÍA MENA, NICOLÁS VILLEGAS SEPÚLVEDA, MACARIO MARTÍNEZ CASTILLO, CÉSAR LÓPEZ-CAMARILLO
Oncology Reports.2016; 35(6): 3696. CrossRef
Autophagy inhibition augments resveratrol-induced apoptosis in Ishikawa endometrial cancer cells
Tomohiko Fukuda, Katsutoshi Oda, Osamu Wada-Hiraike, Kenbun Sone, Kanako Inaba, Yuji Ikeda, Chinami Makii, Aki Miyasaka, Tomoko Kashiyama, Michihiro Tanikawa, Takahide Arimoto, Tetsu Yano, Kei Kawana, Yutaka Osuga, Tomoyuki Fujii
Oncology Letters.2016; 12(4): 2560. CrossRef
Apoptotic Effect of Pinosylvin at a High Concentration Regulated by c-Jun N-Terminal Kinase in Bovine Aortic Endothelial Cells
Jina Song, Jinsun Park, Eunsil Jeong, A-Young So, Jaeho Pyee, Heonyong Park
Journal of Life Science.2015; 25(4): 416. CrossRef
Resveratrol synergistically augments anti-tumor effect of 5-FU in vitro and in vivo by increasing S-phase arrest and tumor apoptosis
Jiening Dun, Xueyan Chen, Haixia Gao, Yan Zhang, Huajun Zhang, Yongjian Zhang
Experimental Biology and Medicine.2015; 240(12): 1672. CrossRef
Pinosylvin at a high concentration induces AMPK-mediated autophagy for preventing necrosis in bovine aortic endothelial cells
Jinsun Park, Jaeho Pyee, Heonyong Park
Canadian Journal of Physiology and Pharmacology.2014; 92(12): 993. CrossRef
Resveratrol promotes endothelial cell wound healing under laminar shear stress through an estrogen receptor-α-dependent pathway
Arif Yurdagul, James J. Kleinedler, Marshall C. McInnis, Alok R. Khandelwal, Allyson L. Spence, A. Wayne Orr, Tammy R. Dugas
American Journal of Physiology-Heart and Circulatory Physiology.2014; 306(6): H797. CrossRef
Protective Effects of Resveratrol on TNF-α-Induced Endothelial Cytotoxicity in Baboon Femoral Arterial Endothelial Cells
Juan Xiao, Jun Song, Vida Hodara, Allen Ford, Xing Li Wang, Qiang Shi, Li Chen, John L. VandeBerg
Journal of Diabetes Research.2013; 2013: 1. CrossRef
Synergistic anti-proliferative effect of resveratrol and etoposide on human hepatocellular and colon cancer cell lines
Fatemehsadat Amiri, Amir-Hassan Zarnani, Hamid Zand, Fariba Koohdani, Mahmood Jeddi-Tehrani, Mohammadreza Vafa
European Journal of Pharmacology.2013; 718(1-3): 34. CrossRef
Cellular stress responses, hormetic phytochemicals and vitagenes in aging and longevity
Vittorio Calabrese, Carolin Cornelius, Albena T. Dinkova-Kostova, Ivo Iavicoli, Rosanna Di Paola, Aleardo Koverech, Salvatore Cuzzocrea, Enrico Rizzarelli, Edward J. Calabrese
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease.2012; 1822(5): 753. CrossRef
Ameliorative Effects of Resveratrol on Acute Ovarian Toxicity Induced by Total Body Irradiation in Young Adult Rats
Yavuz Simsek, Simay Gurocak, Yusuf Turkoz, Nusret Akpolat, Onder Celik, Ali Ozer, Ercan Yılmaz, Ugur Turhan, Fatma Ozyalin
Journal of Pediatric and Adolescent Gynecology.2012; 25(4): 262. CrossRef
Resveratrol Exerts Dosage and Duration Dependent Effect on Human Mesenchymal Stem Cell Development
Lindsay Peltz, Jessica Gomez, Maribel Marquez, Frances Alencastro, Negar Atashpanjeh, Tara Quang, Thuy Bach, Yuanxiang Zhao, Antonio Paolo Beltrami
PLoS ONE.2012; 7(5): e37162. CrossRef
Resveratrol reduces oxidative stress and cell death and increases mitochondrial antioxidants and XIAP in PC6.3-cells
Minna Kairisalo, Alessandra Bonomo, Alise Hyrskyluoto, Giuseppa Mudò, Natale Belluardo, Laura Korhonen, Dan Lindholm
Neuroscience Letters.2011; 488(3): 263. CrossRef
Effect of resveratrol on endothelial cell function: Molecular mechanisms
Christoph A. Schmitt, Elke H. Heiss, Verena M. Dirsch
BioFactors.2010; 36(5): 342. CrossRef
Dose-Dependency of Resveratrol in Providing Health Benefits
Subhendu Mukherjee, Jocelyn I. Dudley, Dipak K. Das
Dose-Response.2010;[Epub] CrossRef
Resveratrol commonly displays hormesis: Occurrence and biomedical significance
Edward J Calabrese, Mark P Mattson, Vittorio Calabrese
Human & Experimental Toxicology.2010; 29(12): 980. CrossRef
Biochemical characterization of the lipid-binding properties of a broccoli cuticular wax-associated protein, WAX9D, and its application
Sun-Young Ahn, Jong-Min Kim, Jae-Ho Pyee, Heon-Yong Park
BMB Reports .2009; 42(6): 367. CrossRef

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Expression of Caspase-3 and c-myc in Non-Small Cell Lung Cancer: Jin young Yoo, Chi Hong Kim, So Hyang Song, Byoung Yong Shim, Youn Ju Jeong, Meyung Im Ahn, Suji Kim, Deog Gon Cho, Min Seop Jo, Kyu Do Cho, Hong Joo Cho, Seok Jin Kang, Hoon Kyo Kim; Cancer Res Treat. 2004;36(5):303-307. Published online October 31, 2004; DOI: https://doi.org/10.4143/crt.2004.36.5.303

Abstract PDF PubReader ePub

Purpose

Caspase-3 is a cysteine protease that plays an important role in the process of apoptotic cell death, but little has been studied clinically on caspase-3 in lung cancer. Increased c-myc expression can result in mitosis or apoptosis, and its contribution to the pathogenesis and prognosis of lung cancer has gained interest. In the present study, the expressions of caspase-3 and c-myc, along with their possible correlations with prognostic variables, were analyzed in resected non-small cell lung carcinomas (NSCLC).

Materials and Methods

Archival tumor tissues from 147 previously untreated NSCLC patients were examined by immunohistochemistry for the expressions of caspase-3 and c-myc proteins. Clinical information was obtained through the computerized retrospective database from the tumor registry.

Results

The expressions of caspase-3 and c-myc were detected in 60 (88/147) and 16% (24/147) of tumors, respectively. No association was found between caspase-3 and c-myc expressions. A multivariate analysis demonstrated the N status and pathologic stage to be significantly correlated with poor survival (p-value=.018 and .002, respectively), but positive expression of caspase-3 was associated with a good prognosis (p=.03).

Conclusion

Our data suggest the involvement of caspase-3 in the tumorigenesis of NSCLC. It is also noteworthy that caspase-3 expression might be a favorable prognostic indicator in these tumors.

Citations

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DNA Damage-Induced Ferroptosis: A Boolean Model Regulating p53 and Non-Coding RNAs in Drug Resistance
Shantanu Gupta, Daner A. Silveira, José Carlos M. Mombach, Ronaldo F. Hashimoto
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Sara Eghtedari, Mahdi Behdani, Fatemeh Kazemi-Lomedasht
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Cancer Cell International.2024;[Epub] CrossRef
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Lina Abdelghany, Chanin Sillapachaiyaporn, Boris Zhivotovsky
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Alev OK ATILGAN, Merih TEPEOĞLU, Eda YILMAZ AKÇAY, Leyla HASANALİYEVA, Dalokay KILIÇ, Handan ÖZDEMİR
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Figen Abatay-Sel, Ayse Erol, Mediha Suleymanoglu, Gokhan Demirayak, Cigdem Kekik-Cinar, Durdane Serap Kuruca, Fatma Savran-Oguz
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Technology in Cancer Research & Treatment.2022;[Epub] CrossRef
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Wen-Bin Zheng, Yang Zou, Jun-Jun He, Hany M. Elsheikha, Guo-Hua Liu, Min-Hua Hu, Shui-Lian Wang, Xing-Quan Zhu
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Hansheng Wu, Shujie Huang, Weitao Zhuang, Guibin Qiao
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Antitumor Effects of Carvacrol and Thymol: A Systematic Review
Laeza Alves Sampaio, Lícia Tairiny Santos Pina, Mairim Russo Serafini, Débora dos Santos Tavares, Adriana Gibara Guimarães
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Daniel Massó-Vallés, Marie-Eve Beaulieu, Laura Soucek
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Synthetic CDCA Derivatives-Induced Apoptosis of Stomach Cancer Cell Line SNU-1 Cells: Bongkyung Moon, Min-Chan Kim, Joo-sung Park; Cancer Res Treat. 2004;36(2):132-139. Published online April 30, 2004; DOI: https://doi.org/10.4143/crt.2004.36.2.132

Abstract PDF PubReader ePub

Purpose

This study was conducted to explore whether CDCA derivatives induce apoptosis in a stomach cancer cell line, and to dissect the detailed mechanism underlying apoptosis.

Materials and Methods

The human stomach cancer cell line, SNU-1, cells were treated with the synthetic CDCA derivatives, HS-1199 and HS-1200. DNA and mitochondrial stains were used to detect apoptotic cells by fluorescence imaging or flow cytometry. The caspase-3 activity was measured by Western blotting.

Results

Both the HS-1199 and HS-1200 induced decreased viabilities of the SNU-1 cells, in time-dependent manners. The CDCA derivatives demonstrated various apoptosis hallmarks, such as mitochondrial changes (reduction of MMP, cytochrome c release, and Smac/ DIABLO translocation), activation of caspase-3 (resulting in the degradation of PARP and DFF45), DNA fragmentation and nuclear condensation.

Conclusion

The CDCA derivatives, HS-1199 and HS-1200, both induced apoptosis of the SNU-1 gastric cancer cells in caspase- and mitochondria-dependent fashions. Many important issues relating to their therapeutic applications remain to be elucidated.

Citations

Citations to this article as recorded by

The anticancer activity of bile acids in drug discovery and development
Weijian Li, Lu Zou, Shuai Huang, Huijie Miao, Ke Liu, Yajun Geng, Yingbin Liu, Wenguang Wu
Frontiers in Pharmacology.2024;[Epub] CrossRef
The Higher Expression of CDCA2 Associated with Poor Prognosis in Glioma
Xin Jin, Zhen-qing Sun, Gui-liang Zhou, Guo-jun Li, Shi-feng Deng, Zhongjie Shi
Disease Markers.2022; 2022: 1. CrossRef
Mechanism of Bile Acid-Induced Programmed Cell Death and Drug Discovery against Cancer: A Review
Jung Yoon Jang, Eunok Im, Yung Hyun Choi, Nam Deuk Kim
International Journal of Molecular Sciences.2022; 23(13): 7184. CrossRef
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Monjur Ahmed
Clinical and Experimental Gastroenterology.2022; Volume 15: 105. CrossRef
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Kulvinder Kochar Kaur, Gautam Nand K. Allahbadia, Mandeep Singh
Journal of Pharmacy and Nutrition Sciences .2022; 12: 35. CrossRef
Ursodeoxycholic acid and cancer: From chemoprevention to chemotherapy
Jean-François Goossens, Christian Bailly
Pharmacology & Therapeutics.2019; 203: 107396. CrossRef

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Effect of Arsenic Trioxide in TRAIL (Tumor Necrosis Factor-related Apoptosis Inducing Ligand)-Mediated Apoptosis in Multiple Myeloma Cell Lines: Jae Ho Byun, Young Seon Hong, Hee Jeong Cheong, Sook Ja Kim, Nam Su Lee, Jong Ho Won, Dae Sik Hong, Hee Sook Park; Cancer Res Treat. 2003;35(6):472-477. Published online December 31, 2003; DOI: https://doi.org/10.4143/crt.2003.35.6.472

Abstract PDF: PURPOSE
The potential therapeutic application of the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), in the treatment of multiple myeloma (MM), was recently proposed. However, there have been some problems with the use of TRAIL, due to the appearance of TRAIL-resistant cells in MM. The effect of arsenic trioxide (As2O3) on the rate of apoptosis induced by TRAIL was evaluated in MM cells.
MATERIALS AND METHODS
Using TRAIL-sensitive (RPMI- 8226) and TRAIL-resistant (ARH-77 and IM-9) MM cell lines, the cell viability, induction of apoptosis, and change in the caspases were examined after treatment with TRAIL alone, or in combination with various concentrations of As2O3.
RESULTS
Incubating the cell lines with As2O3 augmented the TRAIL-induced apoptosis in the MM cell lines, according to the As2O3 concentration. Apoptosis was mediated through caspase activation. When TRAIL was used alone, caspase8 was activated in the RPMI-8226 cell lines, but not in the ARH-77 and IM-9 cell lines. When As2O3 was added to TRAIL, caspase-9 was activated in the ARH-77 and IM-9 cells.
CONCLUSION
The use of As2O3, in combination with TRAIL, would help enhance the level of TRAIL-induced apoptosis, and overcome the TRAIL-resistance, in MM cells.

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TRAIL-Mediated Apoptosis in Human Liver Chang Cells: Channy Park, Sung Wook Hong, Sung Ho Jin, Nam Song Kim, Kyung Ho Cho, Jin Ho Cheon, Jae Yeon Ahn, Jung Ku Yang, Raekil Park; Cancer Res Treat. 2003;35(4):341-348. Published online August 31, 2003; DOI: https://doi.org/10.4143/crt.2003.35.4.341

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PURPOSE
Tumor necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL)/APO-2L is a member of the TNF family that can kill a wide variety of tumor cells, but not normal cells. This study was designed to investigate the down stream target proteins in TRAIL-mediated apoptosis of human liver, Chang cells.
MATERIALS AND METHODS
The expressions of DR4/DR5 in hepatoma cells, including Chang, HepG2 and Hep3B cells, were determined by RT-PCR. Cell viability was measured by MTT assay and apoptosis was assessed by DNA fragmentation assay. The catalytic activity of caspase- family proteases, including caspase-3 and -9, was tested by using fluorogenic biosubstrates. Expression of apoptotic mediators, including procaspase-3 and PARP proteins, was measured by Western blotting. The expression profile of proteins in Chang cells by using two-dimensional (2-D) gel electrophoresis and MALDI-TOF.
RESULTS
The results demonstrated that TRAIL (100 ng/ml) induced the apoptotic death of Chang cells, as characterized by the ladder-pattern fragmentation of genomic DNA. TRAIL increased the enzymatic activity of caspase- 3, corresponding to the time of appearance of cleaved PARP and caspase-9. In 2-D gel electrophoresis and MALDI- TOF analysis, the comparison of control versus apoptotic cells in the protein expressions revealed that signal intensity of 7 spots were decreased, whereas 6 spots were increased among 300 spots. These spots were resolved and identified as a protein information by MALDI-TOF.
CONCLUSION
We suggested that TRAIL induces the apoptotic death of Chang cells via proteome alterations inducing caspase cascade.

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Upregulation of NAD(P)H:Quinone Oxidoreductase By Radiation Potentiates the Effect of Bioreductive β-Lapachone on Cancer Cells
Eun K. Choi, Kaoru Terai, In-Mi Ji, Yeon H. Kook, Kyung H. Park, Eun T. Oh, Robert J. Griffin, Byung U. Lim, Jin-Seok Kim, Doo S. Lee, David A. Boothman, Melissa Loren, Chang W. Song, Heon Joo Park
Neoplasia.2007; 9(8): 634. CrossRef

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Arsenic Trioxide Induces Apoptosis of HL-60 Cells via Activation of Intrinsic Caspase Protease with Mitochondrial Dysfunction: Byung Hak Jung, Channy Park, Hak Ryul Kim, Moo Rim Park; Cancer Res Treat. 2002;34(4):308-315. Published online August 31, 2002; DOI: https://doi.org/10.4143/crt.2002.34.4.308

Abstract PDF

Arsenic trioxide (As2O3) was introduced into the treatment of refractory or relapsed acute promyelocytic leukemia and showed a striking effectiveness in China and United States multicenter study. However, the mechanistic basis for the carcinogenic or therapeutic effects of arsenics is still poorly understood. So, this study is performed to determine whether As2O3 induces apoptosis through intrinsic caspase cascades in acute promyelocytic leukemia HL-60 cells.
MATERIALS AND METHODS
HL-60 cells were treated with As2O3 to investigate apoptosis through signaling of caspase cascades and mitochondrial dysfunction.
RESULTS
As2O3 (>0.5 uM) decreased the viability of HL-60 cells in a dose-dependent manner, which was revealed as apoptosis shown chromatin condensation and ladder pattern DNA fragmentation. As2O3 increased the catalytic activity of caspase family cysteine proteases including caspase-3 and -9 proteases. Consistently, PARP, an intracellular biosubstrate of caspase-3 protease, was cleaved from 116 kDa to 85 kDa fragments. It also induced the change of mitochondrial membrane potential. Morever, As2O3 resulted in the increase of Bak.
CONCLUSION
These data suggest that As2O3 induces apoptosis of HL-60 cells through activation of intrinsic caspase protease with mitochondrial dysfunction.

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The Time‐Dependent Serial Gene Response to Zeocin Treatment Involves Caspase‐Dependent Apoptosis in HeLa Cells
Jooyeon Hwang, Young‐Youl Kim, Sungjin Huh, Junghee Shim, Chan Park, Kuchan Kimm, Dong Kug Choi, Tae‐Kyu Park, Soonhag Kim
Microbiology and Immunology.2005; 49(4): 331. CrossRef

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Phorbol Ester Induced - Apoptosis Mediated by Activating Serine Protease ( s ) and Caspase - 3 / CPP32 in SNU - 16 Human Gastric Cancer Cell Line: I C Park, M J Park, T B Choe, J J Jang, S I Hong, S H Lee; J Korean Cancer Assoc. 2000;32(2):270-278.

Abstract PDF: PURPOSE
Protein kinase C (PKC) is a family of phospholipid dependent serine/threonine protein kinases that have important role in differentiation, development and tumor promotion. PKC also has been reported to be implicated in the induction of apoptosis in a number of studies, but the efforts to define a role for PKC in the induction of apoptosis have been complicated by conflicting reports.
MATERIALS AND METHODS
To determine the effect of phorbol 12-myristate 13-acetate (PMA) on the induction of apoptosis, DNA fragmentation was detected by agarose gel electrophoresis and morphological changes of apoptotic cells were detected by Hoechst 33258 staining. For the detection of caspase-3/CPP32 activity, we used the enzyme substrate Ac-DEVD-pNa and anti- D4-GDI antibody.
RESULTS
In the present study, PMA, a PKC activator, induced apoptosis in SNU-16 human gastric cancer cell line, whose apoptosis was significantly inhibited by the PKC inhibitor, chelerythrine chloride. The caspase-3/CPP32 protease activity was increased in PMA-induced apoptosis. Furthermore, 4-(2-aminoethyl) benzenesulfonyl fluoride (AEBSF), a serine profease inhibitor, also significantly suppressed PMA-induced cell death in an upstream of caspase-3/CPP32.
CONCLUSION
These findings indicate that PMA induces apoptotic cell death in the SNU-16 adenocarcinoma cells through PKC activation, which activates AEBSF-sensitive serine proteases and caspase-3/CPP32. Therefore, our results suggest that PKC would be a potential target for induction of apoptosis.

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Radiation-induced Apoptotic Signaling Pathway in HL - 60 Cells: Sung Ja Ahn, Rae Kil Park, Sang Rock Lee, Woong Ki Chung, Byung Sik Nah, Taek Keun Nam, Hun Taeg Chung, Sun Rock Moon, Heoung Keun Kang, Seung Jin Park; J Korean Cancer Assoc. 2000;32(1):156-167.

Abstract PDF: PURPOSE
The mechanical insights of death of cancer cells by ionizing radiation are not yet clearly defined. Recent evidences have demonstrated that radiation therapy may induce cell death via activation of signaling pathway for apoptosis in target cells. This study was designed whether ionizing radiation may activate the signaling cascades of apoptosis including caspase family cystein proteases, mitogen-activated protein (MAP) kinases, and transcriptional activation factors in target cells eventually leading to death.
MATERIALS AND METHODS
HL-60 cell line in the log phase was used in this study and the culture media was RPMI 1640. The irradiation was done using the linear accelarator and the radiation does was 10 Gy, 20 Gy, and 30 Gy, respectively. The cell viability was tested by MTT assay and apoptosis was identified by the DNA fragmentation assay. JNK1 (cJun N-terminal kinase) and ERK (extracellular-signal regulated protein kinase) activity was analyzed by the in vitro Ig complex kinase assay. NF- kB (Nuclear Factor- kB) and AP-1 (activator protein-1) activity was assayed by the electrophoretic mobility sbift assay.
RESULTS
Ionizing radiation decreased the viability of HL-60 cells in a time and dose dependent manner. Ionizing radiation-induced cell death of HL-60 cells may be an apo- ptotic death which was evidenced as apoptotic characteristic ladder pattern fragmentation of DNA over 20 Gy at 4 hours. Ionizing radiation specifically induced the activation of CPP32-like cystein protease rather than ICE-like protease of HL-60 cells in a time and dose dependent manner. The activation of CPP32-like cystein protease was also evidenced by the digestion of poly (ADP-ribose) polymerase with 30 Gy ionizing irradiation at 2 hours. The activity of JNK1 was transiently increased up to 3.6 fold by 30 Gy ionizing radiation at 2 hours. Ionizing radiation also rapidly activated the transcriptional activation factors including AP-1 and NF- kB at 10 or 30 min.
CONCLUSION
These data suggested that ionizing radiation-induced apoptosis was mediated by the activation of CPP32-like cystein protease, JNK1, and transcriptional activation factors

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