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Review
. 2016 Nov 18;21(11):1566.
doi: 10.3390/molecules21111566.

Biophysical Approach to Mechanisms of Cancer Prevention and Treatment with Green Tea Catechins

Masami Suganuma  1   2 , Atsushi Takahashi  3 , Tatsuro Watanabe  4 , Keisuke Iida  5   6 , Takahisa Matsuzaki  7 , Hiroshi Y Yoshikawa  8 , Hirota Fujiki  9
Affiliations
Review

Biophysical Approach to Mechanisms of Cancer Prevention and Treatment with Green Tea Catechins

Masami Suganuma et al. Molecules. .

Abstract

Green tea catechin and green tea extract are now recognized as non-toxic cancer preventives for humans. We first review our brief historical development of green tea cancer prevention. Based on exciting evidence that green tea catechin, (-)-epigallocatechin gallate (EGCG) in drinking water inhibited lung metastasis of B16 melanoma cells, we and other researchers have studied the inhibitory mechanisms of metastasis with green tea catechins using biomechanical tools, atomic force microscopy (AFM) and microfluidic optical stretcher. Specifically, determination of biophysical properties of cancer cells, low cell stiffness, and high deformability in relation to migration, along with biophysical effects, were studied by treatment with green tea catechins. The study with AFM revealed that low average values of Young's moduli, indicating low cell stiffness, are closely associated with strong potential of cell migration and metastasis for various cancer cells. It is important to note that treatments with EGCG and green tea extract elevated the average values of Young's moduli resulting in increased stiffness (large elasticity) of melanomas and various cancer cells. We discuss here the biophysical basis of multifunctions of green tea catechins and green tea extract leading to beneficial effects for cancer prevention and treatment.

Keywords: AFM; EGCG; adhesion; durotaxis; fluidity; membrane stiffness; metastasis; migration; rigidity; wound healing.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Structures of four green tea catechins and number of their flexible conformations.
Figure 2
Figure 2
Changes in cell stiffness depending on cell-cycle progression in H1299/Fucci cells. The fluorescent color from red (G1 phase), to yellow (G1 to S transition phase), to green (SG2/M phase) and to no color (M to G1 transition phase). Average values of Young’s moduli of cells were determined in each phase by AFM.
Figure 3
Figure 3
Increase in average values of Young’s moduli and inhibition of cell migration depending on the doses of EGCG in B16-F10 cells. EGCG dose-dependently increased cell stiffness and enhanced inhibition of cell migration, but EC did not affect stiffness or cell migration.
Figure 4
Figure 4
Schematic illustration of biophysical understanding of multifunctions of EGCG in relation to “sealing effects of EGCG”.
Figure 5
Figure 5
Treatment with EGCG reduced adhesion of low metastatic (B16-F1) and high metastatic (B16-F10) cells. (A) Bright field and RICM image show adhesion of B16-F1 and B16-F10 cells on the spot of cell-adhesive SAM substrate. The red area (Aχ = 0.48) shows the tight contact area calculated; (B) Bright field and RICM image of B16-F1 and B16-F10 cells treated with 20 μM EGCG; (C) Dose-dependent reduction of tight contact area in B16-F1 (blue line) and B16-F10 (red line) cells by treatment with EGCG. Reprinted with permission from American Chemical Society [71].
Figure 5
Figure 5
Treatment with EGCG reduced adhesion of low metastatic (B16-F1) and high metastatic (B16-F10) cells. (A) Bright field and RICM image show adhesion of B16-F1 and B16-F10 cells on the spot of cell-adhesive SAM substrate. The red area (Aχ = 0.48) shows the tight contact area calculated; (B) Bright field and RICM image of B16-F1 and B16-F10 cells treated with 20 μM EGCG; (C) Dose-dependent reduction of tight contact area in B16-F1 (blue line) and B16-F10 (red line) cells by treatment with EGCG. Reprinted with permission from American Chemical Society [71].
See this image and copyright information in PMC

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