ArticleZhongguo fei ai za zhi = Chinese journal of lung cancer2012
[Effects of tea polyphenols on the expression of NF-κB, COX-2 and survivin in Lewis lung carcinoma xenografts in C57BL/6 mice].
Article in Zhongguo fei ai za zhi = Chinese journal of lung cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 6 citations in OpenAlex.
- Role of Active Components of Medicinal Food in the Regulation of Angiogenesis.Frontiers in pharmacology · 2020Review
- Chemical Composition and Antioxidant, Analgesic, and Anti-Inflammatory Effects of Methanolic Extract ofPain research & management · 2018Article
- Evaluation of anti-inflammatory activity of selected medicinal plants used in Indian traditional medication systemJournal of traditional and complementary medicine · 2016Article
- Anticancer Activity of Saponins from Allium chinense against the B16 Melanoma and 4T1 Breast Carcinoma Cell.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Tea polyphenols induced apoptosis of breast cancer cells by suppressing the expression of Survivin.Scientific reports · 2014Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectiveLung cancer is the leading cause of cancer-related deaths worldwide. The anti-angiogenic effect of tea polyphenols (TPs) on lung carcinoma was confirmed in our previous study. The effect of TPs on the expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), cyclooxygenase-2 (COX-2), and Survivin in Lewis lung cancer xenograft in mice was observed to explore the anti-angiogenic mechanism of TPs.
methodsLewis lung carcinoma was successfully implanted in 32 C57BL/6 mice, which were then randomly divided into the model control group, the Thalidomide group, the TPs group and the TPs combined with Thalidomide group. The tumor inhibition rates in these groups were determined, whereas the expressions of NF-κB, COX-2 and Survivin were detected using immunohistochemical techniques to investigate the molecular mechanism of the anti-tumor effect of TPs.
results(1) The tumor inhibition rates in the Thalidomide control group, the TPs group and the TPs plus Thalidomide group were 17.26%, 20.81%, 44.32% respectively. Compared with the model control group, the tumor inhibition rate was significantly higher in the TPs plus Thalidomide group (P<0.05); (2) Compared with the model control group, the expression of NF-κB was significantly decreased in the TPs group and the TPs plus Thalidomide group, and it was significantly downregulated in the latter (P<0.05); (3) The expression of COX-2 decreased in all treatment groups, and was significantly downregulated in the TPs plus Thalidomide group compared with the model control group (P<0.05); (4) Compared with the model control group, Survivin expression was significantly downregulated in all treatment groups (P<0.05), and was most obviously reduced in the TPs plus the Thalidomide group (P<0.01).
conclusionTPs plus Thalidomide significantly inhibits Lewis lung cancer growth. TPs possibly downregulates the expression of NF-κB, COX-2 and Survivin in tumor tissue, thereby playing important roles in anti-angiogenesis.
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