Nafamostat Mesilate Enhances the Radiosensitivity and Reduces the Radiation-Induced Invasive Ability of Colorectal Cancer Cells.
Hiroshi SuganoYoshihiro ShiraiTakashi HoriuchiNobuhiro SaitoYohta ShimadaKen EtoTadashi UwagawaToya OhashiKatsuhiko YanagaPublished in: Cancers (2018)
Neoadjuvant chemoradiotherapy followed by radical surgery is the standard treatment for patients with locally advanced low rectal cancer. However, several studies have reported that ionizing radiation (IR) activates nuclear factor kappa B (NF-κB) that causes radioresistance and induces matrix metalloproteinase (MMP)-2/-9, which promote tumor migration and invasion. Nafamostat mesilate (FUT175), a synthetic serine protease inhibitor, enhances the chemosensitivity to cytotoxic agents in digestive system cancer cells by inhibiting NF-κB activation. Therefore, we evaluated the combined effect of IR and FUT175 on cell proliferation, migration and invasion of colorectal cancer (CRC) cells. IR-induced upregulation of intranuclear NF-κB, FUT175 counteracted this effect. Moreover, the combination treatment suppressed cell viability and induced apoptosis. Similar effects were also observed in xenograft tumors. In addition, FUT175 prevented the migration and invasion of cancer cells caused by IR by downregulating the enzymatic activity of MMP-2/-9. In conclusion, FUT175 enhances the anti-tumor effect of radiotherapy through downregulation of NF-κB and reduces IR-induced tumor invasiveness by directly inhibiting MMP-2/-9 in CRC cells. Therefore, the use of FUT175 during radiotherapy might improve the efficacy of radiotherapy in patients with CRC.
Keyphrases
- induced apoptosis
- signaling pathway
- locally advanced
- rectal cancer
- nuclear factor
- radiation induced
- pi k akt
- radiation therapy
- neoadjuvant chemotherapy
- squamous cell carcinoma
- phase ii study
- cell proliferation
- oxidative stress
- toll like receptor
- endoplasmic reticulum stress
- cell cycle arrest
- diabetic rats
- high glucose
- early stage
- minimally invasive
- cell migration
- endothelial cells
- combination therapy
- clinical trial
- inflammatory response
- cell cycle
- lymph node
- coronary artery disease
- drug induced
- coronary artery bypass
- percutaneous coronary intervention
- smoking cessation
- stress induced
- replacement therapy
- cell death
- poor prognosis
- nitric oxide