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ABSTRACT: Previous studies showed that JNK signaling pathway activated by LMP1 plays an important role in carcinogenesis of nasopharyngeal carcinoma (NPC). JNK interacting protein (JIP) can inhibit JNK signaling pathway in NPC cell. This study was designed to elucidate the effect of JIP on the proliferation and apoptosis of NPC cells.
After treatment with JIP at different concentrations and time points, the number of proliferating cells were determined by MTT assay; the ability of proliferation of NPC cells was measured by the rate of cloning formation; cell cycle and the apoptotic rate of NPC cells was assayed by flow cytometry.
1. MTT assay showed that cell proliferation was significantly inhibited by JIP in a dose- and time-dependent manner. After treatment with JIP for 24, 48, and 72 hours, the rate of survival cells were 77.8%, 59.2%, and 61.8%, respectively. 2. The number and volume of colonies were decreased after transfection with JIP. 3. The number of cells in S phase was decreased from 25.87% to 19.96%, and the number of cells in G0/G1 phase was elevated from 66.24% to 71.89% after treatment with JIP. 4. In contrast to the control group, the 24 hours apoptotic rate was elevated from 1.25% to 8.25% (about 6.6 times); the 48 hours apoptotic rate was elevated from 1.04% to 31.45% (about 30 times).
The results demonstrated that JIP inhibit the growth of nasopharyngeal carcinoma through arresting the cell cycle at G1/S checkpoint and triggering the apoptosis of cells. Data suggest that JIP is a potent molecular drug for the treatment of the patients with nasopharyngeal carcinoma.
Ai zheng = Aizheng = Chinese journal of cancer 11/2002; 21(11):1182-6.
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ABSTRACT: To elucidate the regulation of the phosphorylation of epidermal growth factor receptor (EGFR) by the EB virus encoded latent membrane protein 1 (LMP1) in nasopharyngeal carcinoma cell line.
The levels of EGFR expression and phosphorylation in pTet-on LMP1 HNE2 cell, a nasopharyngeal carcinoma (NPC) cell line, in the dynamic expression of LMP1 induced by different concentrations of doxycycline (Dox) were observed. The EGFR dominant negative mutant and LMP1 antisense expression plasmid were transiently transfected into pTet-on LMP1 HNE2 cells by lipofectamine, and the changes in EGFR phosphorylation were observed by immunocoprecitation and Western blot. The changes in EGFR phosphorylation were observed after EGF treatment.
In pTet-on LMP1 HNE2 cells, Dox-induced LMP1 upregulated EGFR expression and phosphorylation in a dose-dependent manner. After EGFR dominant negative mutant was transfected into pTet-on LMP1 HNE2 cells, the increase of EGFR phosphorylation was inhibited completely. When LMP1 antisense expression plasmid was transfected into pTet-on LMP1 HNE2 cells, the levels of EGFR phosphorylation were also inhibited significantly. Meanwhile, after EGF had been added into pTet-on LMP1 HNE2 cells, increase of EGFR phosphorylation was induced, but it was completely blocked by EGFR dominant negative mutant and the introduction of LMP1 antisense.
EB virus encoded LMP1 not only induces the dose-dependent expression of EGFR, but also the dose-dependent phosphorylation of EGFR. The phosporylation of EGFR may play a vital role in the development of nasopharyngeal carcinoma.
Zhonghua zhong liu za zhi [Chinese journal of oncology] 06/2002; 24(3):226-9.
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ABSTRACT: Objective: Tea polyphenols present in green tea show cancer chemopreventive effects in many tumor models. Epidemiological
studies have also suggested that green tea consumption might be effective in the prevention of certain human cancers. In the
present study, we investigated the molecular mechanisms of the inhibition of cell proliferation by tea polyphenols in nasopharyngeal
carcinoma (NPC) cell line CNE1-LMP1. Methods: CNE1-LMP1 cells were treated with tea polyphenols at various doses (0, 25, 50,
100, 200 µg/ml) for 24 hours, the morphology of cells was observed by light microscopy, and cell survival rate was determined
by MTT assay. At the same time, cell cycle of CNE1-LMP1 was analyzed by flow cytometry. Cyclin D1 transcription was analyzed
by cyclin D1 promoterluciferase reporter system and expression of cyclin D1 protein by Western blot analysis. Transactivities
of NF-κB and AP-1 was analyzed by Dual-fluorescence reporter gene system. Results: After treatment of CNE1-LMP1 cells with
tea polyphenols, the number of proliferating cells was obviously decreased as determined by light microscopy and MTT assay
(from 100% to 89.4%, 83.3%, 74.8% and 38.1%). With the increase of tea polyphenols concentrations, the number of cells in
S-phase was obviously decreased, and the number of cells in G1-phase from 22.20% to 13.16%, and the number of cells in G0/G1
phase was elevated from 68.5% to 74.08%. It suggests that tea polyphenols could arrest the cell cycle at both of the two checkpoints.
Furthermore, transcription and were obviously declined 7–8 folds (100–200 µg/ml tea polyphenols or EGCG group) and expression
of cyclin D1 protein also decreased in a dose-dependent manner. Transactivities of NF-κB and AP-1 were obviously down-regulated
in CNE1-LMP1 cells. Conclusion: Green tea polyphenols could inhibit cell proliferation, by suppressing the activity of NF-κB
and AP-1, and by down-regulation of the transcription of cyclin D1.
Chinese Journal of Cancer Research 11/2001; 13(4):235-242. · 0.18 Impact Factor
