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Article

Inhibition of proliferation of human lung cancer cells by green tea catechins is mediated by upregulation of let-7

  • Authors:
    • Zhiwei Zhong
    • Zhuo Dong
    • Lihua Yang
    • Xiaoqiang Chen
    • Zhaohui Gong
  • View Affiliations / Copyright

    Affiliations: Institute of Biochemistry and Molecular Biology, School of Medicine, Ningbo University, Ningbo 315211, P.R. China, Hangzhou Tea Research Institute, All China Federation of Supply and Marketing Cooperatives, Hangzhou 310016, P.R. China
  • Pages: 267-272
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    Published online on: May 17, 2012
       https://doi.org/10.3892/etm.2012.580
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Abstract

Green tea catechins are known to function as anticancer agents via inhibition of carcinogenesis during the initiation, promotion and progression stages. Many potential mechanisms have been proposed, yet the precise mechanism of lung cancer prevention by green tea catechins remains unclear. microRNAs (miRs) are a class of 21-24 nucleotide small non-coding RNAs and play critical roles throughout cellular development and regulation. Emerging evidence demonstrates that tea catechins influence the expression of miRs in human cancer cells to inhibit tumorigenesis. Both let-7a-1 and let-7g were detected in the human lung cancer cells treated with tea catechins. The cell viability and cell cycle were analyzed after tea catechins treatment. In the present study, we found that tea catechins upregulated the tumor-suppressor miRs, let-7a-1 and let-7g, in lung cancer cell lines. The upregulation of let‑7a/7g repressed the expression of their targets, C-MYC and the regulatory protein of LIN-28, at the mRNA and protein levels. Moreover, the cell growth assay indicated that tea catechins significantly inhibited cell proliferation, and the flow cytometric analysis revealed an increase in the number of cells in the G2/M phase and a decrease in the number of cells in the S phase after treatment with tea catechins. These observations suggest that green tea catechins mediate the inhibition of proliferation of lung cancer cells through the let-7 signaling pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Zhong Z, Dong Z, Yang L, Chen X and Gong Z: Inhibition of proliferation of human lung cancer cells by green tea catechins is mediated by upregulation of let-7. Exp Ther Med 4: 267-272, 2012.
APA
Zhong, Z., Dong, Z., Yang, L., Chen, X., & Gong, Z. (2012). Inhibition of proliferation of human lung cancer cells by green tea catechins is mediated by upregulation of let-7. Experimental and Therapeutic Medicine, 4, 267-272. https://doi.org/10.3892/etm.2012.580
MLA
Zhong, Z., Dong, Z., Yang, L., Chen, X., Gong, Z."Inhibition of proliferation of human lung cancer cells by green tea catechins is mediated by upregulation of let-7". Experimental and Therapeutic Medicine 4.2 (2012): 267-272.
Chicago
Zhong, Z., Dong, Z., Yang, L., Chen, X., Gong, Z."Inhibition of proliferation of human lung cancer cells by green tea catechins is mediated by upregulation of let-7". Experimental and Therapeutic Medicine 4, no. 2 (2012): 267-272. https://doi.org/10.3892/etm.2012.580
Copy and paste a formatted citation
x
Spandidos Publications style
Zhong Z, Dong Z, Yang L, Chen X and Gong Z: Inhibition of proliferation of human lung cancer cells by green tea catechins is mediated by upregulation of let-7. Exp Ther Med 4: 267-272, 2012.
APA
Zhong, Z., Dong, Z., Yang, L., Chen, X., & Gong, Z. (2012). Inhibition of proliferation of human lung cancer cells by green tea catechins is mediated by upregulation of let-7. Experimental and Therapeutic Medicine, 4, 267-272. https://doi.org/10.3892/etm.2012.580
MLA
Zhong, Z., Dong, Z., Yang, L., Chen, X., Gong, Z."Inhibition of proliferation of human lung cancer cells by green tea catechins is mediated by upregulation of let-7". Experimental and Therapeutic Medicine 4.2 (2012): 267-272.
Chicago
Zhong, Z., Dong, Z., Yang, L., Chen, X., Gong, Z."Inhibition of proliferation of human lung cancer cells by green tea catechins is mediated by upregulation of let-7". Experimental and Therapeutic Medicine 4, no. 2 (2012): 267-272. https://doi.org/10.3892/etm.2012.580
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