TY - JOUR
T1 - Quantitative Evaluation of Cancer Cell Adhesion to Self-Assembled Monolayer-Patterned Substrates by Reflection Interference Contrast Microscopy
AU - Matsuzaki, Takahisa
AU - Ito, Kosaku
AU - Masuda, Kentaro
AU - Kakinuma, Eisuke
AU - Sakamoto, Rumi
AU - Iketaki, Kentaro
AU - Yamamoto, Hideaki
AU - Suganuma, Masami
AU - Kobayashi, Naritaka
AU - Nakabayashi, Seiichiro
AU - Tanii, Takashi
AU - Yoshikawa, Hiroshi Y.
N1 - Funding Information:
The present work was supported by grants from the Japan Society for the Promotion of Science (JSPS) KAKENHI (Nos. 26650046, 23106005, and 15H05351) to H.Y.Y. T.M. acknowledges a Grant-in-Aid for JSPS fellows (No. 25 8820). N.K. gives thanks for a Grant-in-Aid for Young Scientists (B) (No. 26870221). T.T. gives thanks for a Grant-in-Aid for Basic Research (C) (No. 26390035) from the Ministry of Education, Culture, Sports, Science and Technology, Japan.
Publisher Copyright:
© 2016 American Chemical Society.
PY - 2016/2/25
Y1 - 2016/2/25
N2 - Adhesion of cancer cells with different metastatic potential and anticancer drug resistance has been quantitatively evaluated by using self-assembled monolayer (SAM)-patterned substrates and reflection interference contrast microscopy (RICM). Cell-adhesive SAM spots with optimized diameter could prevent cell-cell adhesion and thus allowed the systematic evaluation of statistically reliable numbers of contact area between single cancer cells and substrates by RICM. The statistical image analysis revealed that highly metastatic mouse melanoma cells showed larger contact area than lowly metastatic cells. We also found that both cancer cell types exhibited distinct transition from the "strong" to "weak" adhesion states with increase in the concentration of (-)-epigallocatechin gallate (EGCG), which is known to exhibit cancer preventive activity. Mathematical analysis of the adhesion transition revealed that adhesion of the highly metastatic mouse melanoma cells showed more EGCG tolerance than that of lowly metastatic cells. Moreover, time-lapse RICM observation revealed that EGCG weakened cancer cell adhesion in a stepwise manner, probably via focal adhesion complex. These results clearly indicate that contact area can be used as a quantitative measure for the determination of cancer phenotypes and their drug resistance, which will provide physical insights into the mechanism of cancer metastasis and cancer prevention.
AB - Adhesion of cancer cells with different metastatic potential and anticancer drug resistance has been quantitatively evaluated by using self-assembled monolayer (SAM)-patterned substrates and reflection interference contrast microscopy (RICM). Cell-adhesive SAM spots with optimized diameter could prevent cell-cell adhesion and thus allowed the systematic evaluation of statistically reliable numbers of contact area between single cancer cells and substrates by RICM. The statistical image analysis revealed that highly metastatic mouse melanoma cells showed larger contact area than lowly metastatic cells. We also found that both cancer cell types exhibited distinct transition from the "strong" to "weak" adhesion states with increase in the concentration of (-)-epigallocatechin gallate (EGCG), which is known to exhibit cancer preventive activity. Mathematical analysis of the adhesion transition revealed that adhesion of the highly metastatic mouse melanoma cells showed more EGCG tolerance than that of lowly metastatic cells. Moreover, time-lapse RICM observation revealed that EGCG weakened cancer cell adhesion in a stepwise manner, probably via focal adhesion complex. These results clearly indicate that contact area can be used as a quantitative measure for the determination of cancer phenotypes and their drug resistance, which will provide physical insights into the mechanism of cancer metastasis and cancer prevention.
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U2 - 10.1021/acs.jpcb.5b11870
DO - 10.1021/acs.jpcb.5b11870
M3 - Article
C2 - 26845066
AN - SCOPUS:84959432465
VL - 120
SP - 1221
EP - 1227
JO - Journal of Physical Chemistry B
JF - Journal of Physical Chemistry B
SN - 1520-6106
IS - 7
ER -
