Kwon Mi Ri, Lee Jae Hee, Park Jin, Park Seok Soon, Ju Eun Jin, Ko Eun Jung, Shin Seol Hwa, Son Ga Won, Lee Hye Won, Kim Yeon Joo, Song Si Yeol, Jeong Seong-Yun, Choi Eun Kyung
Department of Medical Science, Asan Medical Institute of Convergence Science and Technology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, 05505, Republic of Korea.
Asan Institute for Life Sciences, ASAN Medical Center, Seoul, 05505, Republic of Korea.
Cell Death Discov. 2023 Jan 13;9(1):7. doi: 10.1038/s41420-023-01303-6.
Metastatic colorectal cancer (CRC) remains a substantial problem for mortality and requires screening and early detection efforts to increase survival. Epithelial-mesenchymal transition (EMT) and circulation of tumor cells in the blood play important roles in metastasis. To identify a novel target for metastasis of CRC, we conducted a gene microarray analysis using extracted RNA from the blood of preclinical models. We found that NCK-associated protein 1 (NCKAP1) was significantly increased in the blood RNA of patient-derived xenograft (PDX) models of colon cancer. In the NCKAP1 gene knockdown-induced human colon cancer cell lines HCT116 and HT29, there was a reduced wound healing area and significant inhibition of migration and invasion. As the result of marker screening for cytoskeleton and cellular interactions, CRC treated with siRNA of NCKAP1 exhibited significant induction of CDH1 and phalloidin expression, which indicates enhanced adherent cell junctions and cytoskeleton. In HCT116 cells with a mesenchymal state induced by TGFβ1, metastasis was inhibited by NCKAP1 gene knockdown through the inhibition of migration, and there was increased CTNNB1 expression and decreased FN expression. We established metastasis models for colon cancer to liver transition by intrasplenic injection shRNA of NCKAP1-transfected HCT116 cells or by implanting tumor tissue generated with the cells on cecal pouch. In metastasis xenograft models, tumor growth and liver metastasis were markedly reduced. Taken together, these data demonstrate that NCKAP1 is a novel gene regulating EMT that can contribute to developing a diagnostic marker for the progression of metastasis and new therapeutics for metastatic CRC treatment.
转移性结直肠癌(CRC)仍然是导致死亡的一个重大问题,需要通过筛查和早期检测来提高生存率。上皮-间质转化(EMT)以及肿瘤细胞在血液中的循环在转移过程中起着重要作用。为了确定CRC转移的新靶点,我们使用从临床前模型血液中提取的RNA进行了基因微阵列分析。我们发现,在结肠癌患者来源的异种移植(PDX)模型的血液RNA中,NCK相关蛋白1(NCKAP1)显著增加。在NCKAP1基因敲低诱导的人结肠癌细胞系HCT116和HT29中,伤口愈合面积减小,迁移和侵袭受到显著抑制。作为细胞骨架和细胞相互作用标记物筛选的结果,用NCKAP1的siRNA处理的CRC表现出CDH1和鬼笔环肽表达的显著诱导,这表明粘附细胞连接和细胞骨架增强。在由TGFβ1诱导的具有间质状态的HCT116细胞中,NCKAP1基因敲低通过抑制迁移来抑制转移,并且CTNNB1表达增加,FN表达减少。我们通过脾内注射NCKAP1转染的HCT116细胞的shRNA或通过将用这些细胞产生的肿瘤组织植入盲肠袋建立了结肠癌肝转移模型。在转移异种移植模型中,肿瘤生长和肝转移明显减少。综上所述,这些数据表明NCKAP1是一种调节EMT的新基因,有助于开发转移进展的诊断标志物和转移性CRC治疗的新疗法。