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Low‐intensity ultrasound differentially upregulates cell death regulators in cancer cells, and downregulates inflammatory pathways in non‐cancer cells via oxidative stresschromatin long‐range interaction signaling
Author(s) -
Yang Qiao,
Wang Jiwei,
Lai Bin,
Sun Yu,
Yu Daohai,
Yang William,
Shao Ying,
Zhang Chunquan,
Liu Yanna,
Wang Hong,
Yang Xiaofeng
Publication year - 2019
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.2019.33.1_supplement.802.82
Subject(s) - cancer cell , programmed cell death , microbiology and biotechnology , carcinogenesis , cancer , biology , chromatin , cancer research , signal transduction , apoptosis , gene , genetics
The mechanisms underlying low intensity ultrasound (LIUS) suppression of inflammations and tumorigenesis remain poorly determined. Here, we determined the mRNA expressions of 299 cell death regulators in 13 cell death types in the microarray data. We made the following findings: 1) LIUS upregulates more cell death regulators in cancer cells than in non‐cancer cells, and downregulates more inflammatory regulators in non‐cancer cells than cancer cells; 2) LIUS‐induced most top signaling pathways in cancer cells are not shared with that in non‐cancer cells. LIUS induces more cell death related pathways in cancer cells but inhibits the expressions of a list of inflammation‐related regulators via TP53‐, and SRF‐, mediated pathways, respectively, in non‐cancer cells; 3) LIUS shares 10–25% of the top pathways with mild hyperthermia in regulating cell death regulator expression regardless of cell types; and shares 15–45% of the top pathways with oscillatory shear stress (OSS) in regulating gene expressions in non‐cancer cells; and 4) LIUS may modulate chromatin long range interactions to regulate gene expressions in cells; upstream chromatin long‐range interaction sites (CLRISs) are more favorable than downstream CLRISs for LIUS modulation of gene expressions in cancer cells; and downstream CLRISs play more important roles than upstream CLRISs for LIUS modulation of gene expressions in non‐cancer cells. Our finding demonstrated that LIUS suppresses tumorigenesis and inhibits inflammation by modulating the expressions of cell death regulators, which leads to novel therapeutic targets for treating cancers and inflammation. Support or Funding Information This work was supported by NIH grant to Drs. XF. Yang, H. Wang. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .