Ishikawa Akira, Fujii Hiroki, Fukui Takafumi, Kido Aya, Katsuya Narutaka, Sentani Kazuhiro, Kuraoka Kazuya, Tazuma Sho, Sudo Takeshi, Serikawa Masahiro, Oka Shiro, Oue Naohide
Department of Molecular Pathology, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan.
Department of Molecular Pathology, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan.
Pathol Res Pract. 2023 Jan;241:154277. doi: 10.1016/j.prp.2022.154277. Epub 2022 Dec 19.
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer and the third leading cause of cancer-related deaths. Therefore, there is an urgent need for a novel molecular target for the treatment of PDAC. Kinesin family member C1 (KIFC1) belongs to the kinesin superfamily proteins and has been reported to be involved in the pathogenesis of a wide variety of carcinomas. However, the role of KIFC1 in PDAC remains unknown. This study aimed to analyze the expression and biological function of KIFC1 in PDAC. Immunohistochemically, KIFC1 was found in 37 of 81 PDAC cases (46%). A high expression of KIFC1 was significantly related to tumor size (p = 0.023) and poor overall survival (p = 0.011). Univariate and multivariate analysis indicated that KIFC1 expression was a prognostic factor in PDAC cases. As for cancer stem cell markers, KIFC1 expression tended to co-express significantly with CD44 (p < 0.01). The growth and spheroid colony formation of KIFC1 small interfering RNA (siRNA)-transfected PDAC cells were significantly lower than those of negative control siRNA-transfected cells. Therefore, our findings suggest that KIFC1 is an independent prognostic factor in PDAC and may represent a new promising therapeutic target in PDAC.
胰腺导管腺癌(PDAC)是一种侵袭性癌症,是癌症相关死亡的第三大主要原因。因此,迫切需要一种用于治疗PDAC的新型分子靶点。驱动蛋白家族成员C1(KIFC1)属于驱动蛋白超家族蛋白,据报道其参与多种癌症的发病机制。然而,KIFC1在PDAC中的作用仍不清楚。本研究旨在分析KIFC1在PDAC中的表达及生物学功能。免疫组织化学检测发现,81例PDAC病例中有37例(46%)存在KIFC1表达。KIFC1的高表达与肿瘤大小显著相关(p = 0.023),与总体生存率低显著相关(p = 0.011)。单因素和多因素分析表明,KIFC1表达是PDAC病例的一个预后因素。至于癌症干细胞标志物,KIFC1表达倾向于与CD44显著共表达(p < 0.01)。KIFC1小干扰RNA(siRNA)转染的PDAC细胞的生长和球状体集落形成明显低于阴性对照siRNA转染的细胞。因此,我们的研究结果表明,KIFC1是PDAC的一个独立预后因素,可能是PDAC中一个新的有前景的治疗靶点。