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Extracellular matrix (ECM)‐stiffness regulated cancer cell (A549) migration
Author(s) -
Gweon Bomi,
Li Zeyuan,
Shin Yujin,
Yoo Hongki,
Shin Jennifer H.
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.923.3
Subject(s) - extracellular matrix , cell migration , a549 cell , microbiology and biotechnology , population , chemistry , cytoskeleton , cell , mesenchymal stem cell , biophysics , biology , medicine , biochemistry , environmental health
Extracellular matrix (ECM)‐stiffness is one of the potent regulator of cell physiology such as proliferation, morphology, and migration. From previous studies, it has been known that tumor develops increased collagen deposition at the surrounding tissues. The presence of this dense collagen matrix is shown to promote tissue‐stiffening and, further, metastatic outcomes. However, little is known about how this mechanical stimulation, ECM‐stiffening, are transduced into cells and derive tumor progression. To investigate the relationship, we grew human lung carcinoma cells (A549) on the collagen coated ECM synthesized by polyacrylamide with physiologically relevant range stiffness (0.3 ~ 150 kPa). We chose A549 cells because A549s are reported to be sensitive to ECM‐stiffness. To correlate the ECM‐stiffness to metastatic behavior of cells, we observed migration of cells under microscope for about 24 hours equipped with incubator. In order to track the path of individual cell movement, we kept the cell population in sparse condition during this 24 hours. When we measured the migration speed, cells on soft substrate (0.3 kPa) migrated relatively slower compare to the ones on stiffer substrate (19 kPa and 153 kPa). Cells, also, tend to spread slightly less on soft substrate (0.3 kPa). To determine if these alterations in cell physiological induced by ECM‐stiffness change is related to cytoskeletal contractility, we additionally measured cellular traction. Support or Funding Information This work was supported by the National Research Foundation of Korea Grant funded by the Korean Government (NRF‐2014R1A6A3A04059713 and NRF‐2013S1A2A2035518).