CCT6A 在结直肠癌中具有良好的诊断生物标志物功能,并能促进细胞增殖。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
ACS Applied Electronic Materials Pub Date : 2024-09-16 eCollection Date: 2024-01-01 DOI:10.7150/jca.98901
Jianxing Ma, Qiuya Wei, Lili Zhang, Fengyao Sun, Wen Li, Ruihang Du, Mingchan Liu, Siyuan Yan, Chen Wang
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引用次数: 0

摘要

背景:含伴侣素无尾复合体多肽 1 亚基 6A(CCT6A)主要位于细胞质中,被认为参与了肿瘤的各种生物学过程。然而,其功能和内在机制有待进一步阐明。研究方法采用多组学分析评估CCT6A表达与患者预后的相关性及其免疫价值。通过 CRISPR-Cas9 敲除 CCT6A,并通过转染质粒使其在结直肠癌(CRC)细胞中过表达。细胞增殖通过 MTS、EDU 染色和集落生长试验进行分析,细胞迁移通过伤口愈合试验和 Transwell 试验进行监测。研究人员还利用磷酸激酶阵列试剂盒和免疫印迹分析法探讨了潜在的分子机制。结果发现CCT6A在多种肿瘤组织中高表达,并与患者的预后显著相关。它还与 CRC 的免疫浸润、免疫相关性和预后有关。CCT6A 在 CRC 活检组织和新鲜 CRC 组织中均有高表达。同时,敲除 CCT6A 会减少细胞增殖、细胞周期和细胞迁移。相反,过表达 CCT6A 则表现出相反的表型。此外,我们还发现在 CCT6A 过表达的细胞中,HSPD1 和非磷酸化 P53 高度增加,它们参与了肿瘤发生的调控。结论因此,CCT6A 能正向调节 CRC 细胞的增殖/迁移,并表明 CCT6A 具有较高的免疫学价值,且与 CRC 的进展相关,这使其成为 CRC 的潜在治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
CCT6A functions as promising diagnostic biomarker and promotes cell proliferation in colorectal cancer.

Background: Chaperonin-containing tailless complex polypeptide 1 subunit 6A (CCT6A) is mainly located in the cytoplasm and considered to be involved in various biological processes in tumors. However, its function and the intrinsic mechanism need to be further elucidated. Methods: Multi-omics analysis was used to evaluate the correlation between CCT6A expression and prognosis of patients, as well as its immune value. CCT6A was knockout by CRISPR-Cas9, and overexpressed by transfecting plasmids in colorectal cancer (CRC) cells. Cell proliferation was analyzed by MTS, EDU staining and colony growth assay, and cell migration was monitored by wound healing assay and Transwell assay. The phosphor-kinase array kit and immunoblotting assay was utilized to explore the potential molecular mechanisms. Results: CCT6A was highly expressed in multiple tumor tissues and significantly correlated with the prognosis of patients. It was also associated with the immune infiltration, immune correlation and prognosis in CRC. CCT6A was highly expressed in CRC biopsies as well as fresh CRC tissues. Meanwhile, knockout of CCT6A reduced cell proliferation, cell cycle and cell migration. On the contrary, overexpression of CCT6A exhibited the opposite phenotypes. Moreover, we identified that HSPD1 and non-phosphorylated P53 were highly increased in CCT6A overexpressed cells, which are involved in regulating tumorigenesis. Conclusions: Therefore, CCT6A positively regulated cell proliferation/migration in CRC cells, and suggesting CCT6A has a high immunological value and is associated with CRC progression, which makes it a potential therapeutic target for CRC.

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来源期刊
CiteScore
7.20
自引率
4.30%
发文量
567
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