[Cyclooxygenase-2 expression in esophageal cancer cells and induction by mitomycin C].
OBJECTIVE
To study the relationship between COX-2 expression in esophageal cancer cell (EC/CUHK-1) and mitomycin C (MMC) treatment.


METHODS
2 mg/L of MMC was added to the well-grown EC/CUHK-1 cells cultured in RPMI-1640 including 10% FCS, and the medium was totally changed after 0.5, 1, 2, 4 and 8 h treatment, respectively. Cells were collected after another 24 h culture. Protein expression of COX-2, Bcl-2, Rb, p53 were examined by Western blot, and RT-PCR method was used to confirm the COX-2 expression in mRNA level. Cell cycle analysis for cells collected at 0, 0.5, 2, 4 and 8 h was performed on an EPICS profile analyzer.


RESULTS
The cell cycle analysis showed that the percentage of apoptosis cells were (4.12 +/- 0.83)%, (1.00 +/- 0.11)%, (4.32 +/- 0.99)%, (9.46 +/- 2.11)% and (31.10 +/- 3.57)%, respectively. COX-2 mRNA expression were 2.60, 1.70, and 0.08 times, COX-2 protein expression were 2.0, 3.1 and 2.8 times, Bcl-2 protein were 3.6, 14.0 and 12.0 times, p53 protein were 1.8, 0.5 and 0.2 times, hyperphosphorylated form Rb were 8.2, 8.4 and 6.2 times, underphosphorylated form Rb were 1.8, 0.5 and 0.2 times in 0.5, 2 and 4 h after MMC treatment, respectively, as compared with the control group.


CONCLUSIONS
The COX-2 expression showed coincidence up-regulation according to the MMC-induced anti-apoptosis function activation in esophageal cancer cells, and the process was at least partly associated with Rb phosphorylation and p53 accumulation. It is implied that COX-2 may be a protecting factor in MMC induced esophageal cancer cell apoptosis, and the use of COX-2 inhibitor as an enhancer for esophageal cancer chemotherapy may be reasonable.
Zhuang
Ze-hao
ZH
Laboratory for Cancer Research, College of Medicine, Zhengzhou University, Zhengzhou 450052, China.
Wang
Li-dong
LD
Tsao
Sai-wah
SW
Cheung
Lai-man
LM
Feng
Hui-chen
HC
Yang
Ting
T
Qin
Yan-ru
YR
Wang
Cheng-dang
CD
Chen
Zhi-zhe
ZZ
Liu
Bin
B
D000903:Antibiotics, Antineoplastic / Q000494:pharmacology*; D017209:Apoptosis; D051546:Cyclooxygenase 2; D004938:Esophageal Neoplasms / Q000201:enzymology / Q000473:pathology; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects*; D006801:Humans; D007527:Isoenzymes / Q000235:genetics / Q000378:metabolism*; D008565:Membrane Proteins; D016685:Mitomycin / Q000494:pharmacology*; D011451:Prostaglandin-Endoperoxide Synthases / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000187:drug effects / Q000378:metabolism; D016160:Retinoblastoma Protein / Q000378:metabolism; D014407:Tumor Cells, Cultured; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D015854:Up-Regulation / Q000187:drug effects
D000903:Antibiotics, Antineoplastic; D007527:Isoenzymes; D008565:Membrane Proteins; D012333:RNA, Messenger; D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53; D016685:Mitomycin; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases