Iseki Yasuhito, Shibutani Masatsune, Maeda Kiyoshi, Nagahara Hisashi, Fukuoka Tatsunari, Matsutani Shinji, Hirakawa Kosei, Ohira Masaichi
Department of Surgical Oncology, Osaka City University Graduate School of Medicine, Osaka, Japan.
Department of Surgical Oncology, Osaka City University Graduate School of Medicine, Osaka, Japan
Anticancer Res. 2018 Apr;38(4):2031-2035. doi: 10.21873/anticanres.12442.
miR-96 is reported to inhibit reversion cysteine-rich Kazal motif (RECK), which is associated with tumor invasion, in solid cancer types (e.g. breast cancer, non-small cell lung cancer, esophageal cancer). The purpose of this study is to clarify whether miR-96 is similarly associated with tumor invasion in colorectal cancer.
We performed western blotting to investigate the expression of RECK when miR-96 mimics or inhibitors were transferred into HCT-116 colorectal cancer cells. The RECK mRNA level was assessed by a reverse transcription polymerase chain reaction. An invasion assay was used to evaluate tumor invasion.
The expression of RECK was inhibited by the transfection of miR-96 mimics. RECK mRNA level was reduced by miR-96 mimics and increased by miR-96 inhibitor. In the invasion assay, miR-96 mimics were shown to promote tumor invasion.
miR-96 may be associated with tumor invasion through inhibition of RECK expression in colorectal cancer.
据报道，在实体癌类型（如乳腺癌、非小细胞肺癌、食管癌）中，miR-96可抑制与肿瘤侵袭相关的富含半胱氨酸的Kazal基序（RECK）。本研究旨在阐明miR-96在结直肠癌中是否同样与肿瘤侵袭相关。
我们进行了蛋白质印迹分析，以研究当将miR-96模拟物或抑制剂转入HCT-116结直肠癌细胞时RECK的表达情况。通过逆转录聚合酶链反应评估RECK mRNA水平。采用侵袭实验评估肿瘤侵袭。
miR-96模拟物转染可抑制RECK的表达。miR-96模拟物使RECK mRNA水平降低，而miR-96抑制剂使其升高。在侵袭实验中，miR-96模拟物可促进肿瘤侵袭。
在结直肠癌中，miR-96可能通过抑制RECK表达与肿瘤侵袭相关。
