Mechanical Stress Downregulates MHC Class I Expression on Human Cancer Cell Membrane
AuthorsLa Rocca, Rosanna
Talib Hassan, Almosawy
Di Fabrizio, Enzo M.
KAUST DepartmentPhysical Sciences and Engineering (PSE) Division
Biological and Environmental Sciences and Engineering (BESE) Division
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AbstractIn our body, cells are continuously exposed to physical forces that can regulate different cell functions such as cell proliferation, differentiation and death. In this work, we employed two different strategies to mechanically stress cancer cells. The cancer and healthy cell populations were treated either with mechanical stress delivered by a micropump (fabricated by deep X-ray nanolithography) or by ultrasound wave stimuli. A specific down-regulation of Major Histocompatibility Complex (MHC) class I molecules expression on cancer cell membrane compared to different kinds of healthy cells (fibroblasts, macrophages, dendritic and lymphocyte cells) was observed, stimulating the cells with forces in the range of nano-newton, and pressures between 1 and 10 bar (1 bar = 100.000 Pascal), depending on the devices used. Moreover, Raman spectroscopy analysis, after mechanical treatment, in the range between 700–1800 cm−1, indicated a relative concentration variation of MHC class I. PCA analysis was also performed to distinguish control and stressed cells within different cell lines. These mechanical induced phenotypic changes increase the tumor immunogenicity, as revealed by the related increased susceptibility to Natural Killer (NK) cells cytotoxic recognition.
CitationLa Rocca R, Tallerico R, Talib Hassan A, Das G, Tadepally L, et al. (2014) Mechanical Stress Downregulates MHC Class I Expression on Human Cancer Cell Membrane. PLoS ONE 9(12): e111758. doi:10.1371/journal.pone.0111758
SponsorsEnnio Carbone's work has been supported by a UICC International Cancer Technology Transfer Fellowship, grant AIRC-IG 10189, and grant AIRC 15521. Rossana Tallerico is a Post Doc awarded by triennial fellowships “Luciana Selce” FIRC. Giovanni Cuda has been supported by PON01_02834 Prometeo (Ministry of Education and Research) and PONa3_00435 Biomedpark@UMG (Ministry of Education and Research). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
PublisherPublic Library of Science (PLoS)
PubMed Central IDPMC4277281
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