Hydrodynamic shear stress promotes epithelial-mesenchymal transition by downregulating ERK and GSK3β activities.
Hye Yeon ChoiGwang-Mo YangAhmed Abdal DayemSubbroto Kumar SahaKyeongseok KimYoungbum YooKwonho HongJin-Hoi KimCassian YeeKyung-Mi LeeSsang-Goo ChoPublished in: Breast cancer research : BCR (2019)
Fluid shear stress experienced during systemic circulation of human breast tumor cells can lead to specific acquisition of mesenchymal stem cell (MSC)-like potential that promotes EMT, mesenchymal-epithelial transition, and metastasis to distant organs. Our data revealed that biomechanical forces appeared to be important microenvironmental factors that not only drive hematopoietic development but also lead to acquisition of CSLCs/TIC potential in cancer metastasis. Our data highlight that +SS is a critical factor that promotes the conversion of CTCs into distinct TICs in blood circulation by endowing plasticity to these cells and by maintaining their self-renewal signaling pathways.
Keyphrases
- epithelial mesenchymal transition
- signaling pathway
- induced apoptosis
- bone marrow
- pi k akt
- mesenchymal stem cells
- electronic health record
- endothelial cells
- cell cycle arrest
- transforming growth factor
- stem cells
- big data
- lymph node
- cell proliferation
- single cell
- cell death
- endoplasmic reticulum stress
- climate change
- data analysis