Sugano Hiroshi, Shirai Yoshihiro, Horiuchi Takashi, Saito Nobuhiro, Shimada Yohta, Eto Ken, Uwagawa Tadashi, Ohashi Toya, Yanaga Katsuhiko
Department of Surgery, The Jikei University School of Medicine, 3-25-8, Nishi-Shinbashi, Minato-ku, Tokyo 105-8461, Japan.
Division of Gene Therapy, Research Center for Medical Science, The Jikei University School of Medicine, 3-25-8, Nishi-Shinbashi, Minato-ku, Tokyo 105-8461, Japan.
Cancers (Basel). 2018 Oct 17;10(10):386. doi: 10.3390/cancers10100386.
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.
新辅助放化疗后行根治性手术是局部晚期低位直肠癌患者的标准治疗方法。然而,多项研究报告称,电离辐射(IR)可激活核因子κB(NF-κB),导致放射抗性并诱导基质金属蛋白酶(MMP)-2/-9,从而促进肿瘤迁移和侵袭。甲磺酸萘莫司他(FUT175)是一种合成的丝氨酸蛋白酶抑制剂,通过抑制NF-κB激活来增强消化系统癌细胞对细胞毒性药物的化学敏感性。因此,我们评估了IR和FUT175联合对结肠直肠癌(CRC)细胞增殖、迁移和侵袭的影响。IR诱导的核内NF-κB上调,FUT175可抵消这种作用。此外,联合治疗可抑制细胞活力并诱导凋亡。在异种移植肿瘤中也观察到了类似的效果。此外,FUT175通过下调MMP-2/-9的酶活性来阻止IR引起的癌细胞迁移和侵袭。总之,FUT175通过下调NF-κB增强放疗的抗肿瘤作用,并通过直接抑制CRC细胞中的MMP-2/-9降低IR诱导的肿瘤侵袭性。因此,放疗期间使用FUT175可能会提高CRC患者放疗的疗效。