期刊
JOURNAL OF CELL BIOLOGY
卷 210, 期 4, 页码 583-594出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201502039
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资金
- National Institute of General Medical Sciences [GM50009]
- National Institutes of Health Training program in Cancer Pharmacology [R25CA1485052-02]
- National Science Foundation [ECCS-0335765]
- National Institutes of Health awards [R01 HL082792]
- Department of Defense Breast Cancer Idea Award [BC102152]
- National Science Foundation CAREER award [CBET-1254846]
- Cornell Center on the Microenvironment and Metastasis from National Cancer Institute [U54CA143876]
- National Cancer Institute [CA129359]
- CDMRP [545346, BC102152] Funding Source: Federal RePORTER
- Div Of Chem, Bioeng, Env, & Transp Sys
- Directorate For Engineering [1254846] Funding Source: National Science Foundation
Non-muscle myosin II (NMII) is reported to play multiple roles during cell migration and invasion. However, the exact biophysical roles of different NMII isoforms during these processes remain poorly understood. We analyzed the contributions of NMIIA and NMIIB in three-dimensional (3D) migration and in generating the forces required for efficient invasion by mammary gland carcinoma cells. Using traction force microscopy and microfluidic invasion devices, we demonstrated that NMIIA is critical for generating force during active protrusion, and NMIIB plays a major role in applying force on the nucleus to facilitate nuclear translocation through tight spaces. We further demonstrate that the nuclear membrane protein nesprin-2 is a possible linker coupling NMIIB-based force generation to nuclear translocation. Together, these data reveal a central biophysical role for NMIIB in nuclear translocation during 3D invasive migration, a result with relevance not only to cancer metastasis but for 3D migration in other settings such as embryonic cell migration and wound healing.
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