바로가기메뉴

본문 바로가기 주메뉴 바로가기

Tuberculosis & Respiratory Diseases

Article Contents

Prev Next
e-Submission

Vol.56 No.4
Citation Share

Inducing Apoptosis of NCl-H157 Humman Lung Carcinoma Cells via Activation of Caspase Cascade by Combination Treatment with ArsenicTrioxide and Sulindac

Tuberculosis & Respiratory Diseases / Tuberculosis & Respiratory Diseases,
2004, v.56 no.4, pp.381-392



& (2004). Inducing Apoptosis of NCl-H157 Humman Lung Carcinoma Cells via Activation of Caspase Cascade by Combination Treatment with ArsenicTrioxide and Sulindac. Tuberculosis & Respiratory Diseases, 56(4), 381-392.
  • Downloaded
  • Viewed
PDF Download

Abstract

Arsenic trioxide(As2O3) was introduced into the treatment of refractory or relapsed acute promyelocytic leukemia. Some investigators have reported that arsenic trioxide had induced apoptosis in a variety of solid human tumor cell lines, including non-small cell lung cancer. Non-steroidal anti-inflammatory drugs(NSAIDs) are powerful chemopreventive agents for gastrointestinal cancers and the growth of established tumors are reduced by inducing apoptosis. It's also reported that NSAIDs enhanced tumor response to chemotherapeutic drugs or radiation. In this study, we aimed to determine whether combination of arsenic trioxide with sulindac augmented its apoptotic potential in NCI-H157 human lung cancer cells. The human lung cancer cell line NCI-H157 was treated with arsenic trioxide and sulindac. Cell viability was measured by the MTT assay. Apoptosis was measured by nuclear staining and flow cytometric analysis. The catalytic activity of the caspase families were measured by the fluorogenic cleavage of biosubstrates. The western blotting were also performed to define the mechanical basis of apoptosis.Combination treatment of arsenic trioxide and sulindac decreased the viability of NCI-H157 human lung cancer cells in a dose-dependent manner. The catalytic activity of caspase-3, 8 and 9 proteases were increased after combination treatment. Consistently PARP was cleaved from 116kDa to 85kDa fragments, and the expression of ICAD was decreased by time-dependent manner. Also combination treatment increased the expression of Fas and Fas/L.Combination therapy of arsenic trioxide with sulindac augments cell death and induces apoptosis via the activation of caspase cascade in NCI-H157 human lung carcinoma cells.(Tuberculosis and Respiratory Diseases 2004, 56:381-392)

keywords
Arsenic trioxide, Sulindac, Apoptosis, Lung Cancer Cell line.

Reference

1.

Chen CJ, (sclerosis1988) genecity of high-arsenicartesian well water Multiple risk factors and related malignant neoplasm of blackfoot disease,

2.

Chen CJ, (1992) Cancer potential in liver,lung,bladder and kidney due to ingested inorganic arsenic in drinking water,

3.

Sun HD, (1992) Treatment of acute promyelocytic leukemia by Ailing-1 therapy with use of syndrome differentiation of traditional Chinese medicine,

4.

Soignet SL, (2001) United States multicenter study of arsenic trioxide in relapsed acute promyelocytic leukemi,

5.

Ling YH, (2002) Arsenic trioxide produces polymerization of microtubules and mitotic arrest before apoptosis in human tumor cell lines,

6.

Shen ZY, (1999) Arsenic trioxide induces apoptosis of oesophageal carcinoma in vitro,

7.

Akao Y, (1992) Arsenic trioxide induces apoptosis in neuroblastoma cell lines through the activation of caspase 3 in vitro,

8.

Seol JG, (1999) Effect of arsenic trioxide on cell cycle arrest in head and neck cancer cell line PCI-1,

9.

Zheng J, (1999) Arsenic trioxide incuces apoptosis of HPV16 DNA-immortalized human cervical epithelial cells and selectively inhibits viral gene expression,

10.

Zhang TC, (1999) Induction of apoptosis and inhibition of huꠀman gastric cancer MGC-803 cell growth by arsenic trioxide,

11.

Thun MJ, (1991) Aspirin use and reduced risk of fatal colon cancer,

12.

Harris RE, (1996) Nonsteroidal antiinflammatory drugs and breꠀast cancer,

13.

Everson RB, (epidemiology1994) dence in a prospective study, Scheinemachers DM

14.

Smalley WE, (1997) Colorectal cancer and non-steroidal anti-inflammatory drugs,

15.

Dannenberg AJ, (1999) Chemoprevention of colon-rectal cancer through inhibition of cyclooxygenase-2,

16.

Shiff SJ, (1995) Sulindac sulfide, an aspirin-like compound, inhibits proliferation, causes cell cycle quiescence, and induces apoptosis in HT-29 colon adenoꠀcarcinoma cells,

17.

Chan TA, (1998) Mechanism underlying nonsteroidal antiinflammatory drug-mediated apoptosis,

18.

Klampfer L, (1999) Sodium salicylate activates caspases and induces apoptosis of myeloid leukemia cell lines,

19.

Milas L, (2001) Cyclooxygenase-2 (COX-2) enzyme inhibitors as potential enhancers of tumor radioresponse,

20.

Koki AT, (1999) Potential utility of COX-2 inhibitors in chemopreꠀvention and chemotherapy,

21.

Milas L, (1999) Enhancement of tumor response to gamma-radiation by an inhibitor of cyclooxygenase-2 enzyme,

22.

Williams GT, (1994) Apoptosis in the immune system,

23.

Cohen JJ, (1993) Apoptosis:the physiologic pathway of cell death,

24.

Chen GQ, (1997) Use of arsenic trioxide (As2O3) in the treatment of acute promyeꠀlcytic leukemia(APL) I. As2O3 exerts dose- dependent dual effects on APL cells,

25.

Chen GQ, (1996) In vitro studies on cellular and molecular mechanisms of arsenic trioxide in the treatment of acute promyelocytic leuꠀkemia: arsenic trioxide induces NB4 cell apoptosis with downregualation of Bcl-2 expression and modulation of PML-RAR/PML proteins,

26.

Uslu R, (2000) Arsenic trioꠀxide-mediated cytotoxicity and apoptosis in prostate and ovarian carcinoma cell lines,

27.

Jung BH, (2002) Arseꠀnic trioxide induces apoptosis of HL-60 cells via activation of intrinsic caspase protease with mitochondrial dysfunction,

28.

Huang S, (2000) Induction of mitosis-mediated apoptosis by sodium arseꠀnite in Hela S3 cells,

29.

Park WH, (2000) Arsenic trioxide-mediated growth inhibition in MC/CAR myeloma cells via cell cycle arrest in association with induction of cyclin-dependent kinase inhibiꠀtor, p21, and apoptosis,

30.

Torrance CJ, (2000) Combinatorial chemoprevention of intestinal neoplasia,

31.

Duffy CP, (1998) Enhancement of chemotherapeutic drug toxicity to human tumour cells in vitro by a subset of NSAIDs,

32.

Soriano AF, (1999) Synergistic effects of new chemopreventive agents and conventional cytotoxic agents against human lung cancer cell lines,

33.

Hida T, (2000) Cyclooxyꠀgenase-2 inhibitor induces apoptosis and enhances cytotoxicity of various anticancer agents in non-small cell lung cancer cell lines,

Tuberculosis & Respiratory Diseases

e-Submission OA Policy