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对……的抑制作用可抑制人甲状腺乳头状癌细胞的恶性增殖。 (你提供的原文似乎不完整,“Suppression of”后面缺少具体内容)

Suppression of inhibits malignant proliferation of human papillary thyroid carcinoma cell.

作者信息

Shi Xiaohui, Cheng Suisheng, Wang Weixing

机构信息

Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.

Department of Thyroid Tumor Surgery, Tumor Center, Inner Mongolia Autonomous Region People's Hospital, Hohhot, Inner Mongolia 010000, P.R. China.

出版信息

Oncol Lett. 2018 Jun;15(6):9202-9208. doi: 10.3892/ol.2018.8496. Epub 2018 Apr 13.

DOI:10.3892/ol.2018.8496
PMID:29805652
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5958781/
Abstract

Papillary thyroid carcinoma (PTC) is the most frequently occurring subtype of thyroid cancer. A certain portion of PTCs can progress to recurrent metastatic cancer. Currently, there remains no effective molecular target therapy for PTCs. As a subunit of the chaperonin containing TCP1 (CCT) complex, is involved in various biological processes. has been reported to drive the proliferation of hepatocellular carcinoma cells. Nevertheless, it remains unknown whether regulates the development of PTC. The present study examined CCT3 protein expression in 30 PTC samples from patients undergoing thyroidectomy. A significant increase was observed in CCT3 expression in the PTC samples compared with the matched adjacent normal thyroid tissues. Lentiviral-mediated small interfering RNAs were used to knock down in K1 cells. It was observed that the expression of was significantly suppressed in K1 cells infected with lentivirus containing a -targeting short hairpin RNA. Our results showed that knockdown markedly decreased the proliferation and cell cycle progression of K1 cells. In addition, the knockdown of induced apoptosis of K1 cell. Taken together, the findings of the present study indicated that CCT3 presents as a potential molecular marker of PTC and regulates the development of PTC in humans.

摘要

甲状腺乳头状癌(PTC)是甲状腺癌中最常见的亚型。一部分PTC会进展为复发性转移性癌。目前,对于PTC尚无有效的分子靶向治疗方法。作为含TCP1的伴侣蛋白(CCT)复合体的一个亚基, 参与多种生物学过程。据报道, 可驱动肝癌细胞的增殖。然而, 是否调节PTC的发展仍不清楚。本研究检测了30例接受甲状腺切除术患者的PTC样本中CCT3蛋白的表达。与匹配的相邻正常甲状腺组织相比,PTC样本中CCT3表达显著增加。采用慢病毒介导的小干扰RNA敲低K1细胞中的 。观察到,在感染了含靶向 短发夹RNA的慢病毒的K1细胞中, 的表达显著受到抑制。我们的结果表明,敲低 显著降低了K1细胞的增殖和细胞周期进程。此外,敲低 诱导了K1细胞凋亡。综上所述,本研究结果表明,CCT3是PTC的一个潜在分子标志物,并调节人类PTC的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f0c/5958781/bc1a7d13fe9c/ol-15-06-9202-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f0c/5958781/f22b4359791b/ol-15-06-9202-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f0c/5958781/6c2f19daf2cd/ol-15-06-9202-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f0c/5958781/529ee7ba59ce/ol-15-06-9202-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f0c/5958781/e3660f8a7884/ol-15-06-9202-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f0c/5958781/bc1a7d13fe9c/ol-15-06-9202-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f0c/5958781/f22b4359791b/ol-15-06-9202-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f0c/5958781/6c2f19daf2cd/ol-15-06-9202-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f0c/5958781/529ee7ba59ce/ol-15-06-9202-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f0c/5958781/e3660f8a7884/ol-15-06-9202-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f0c/5958781/bc1a7d13fe9c/ol-15-06-9202-g04.jpg

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