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慢病毒介导的三重基序68的RNA干扰抑制结肠癌细胞系SW1116和HCT116的增殖。

Lentivirus-mediated RNA interference of tripartite motif 68 inhibits the proliferation of colorectal cancer cell lines SW1116 and HCT116 .

作者信息

Tan Zhen, Liu Xiaoshuang, Yu Enda, Wang Hantao, Tang Lijun, Wang Hao, Fu Chuangang

机构信息

Department of Colorectal Surgery, Changhai Hospital, Second Military Medical University, Shanghai 200433, P.R. China.

PLA Center of General Surgery, Chengdu Military General Hospital, Chengdu, Sichuan 610083, P.R. China.

出版信息

Oncol Lett. 2017 Apr;13(4):2649-2655. doi: 10.3892/ol.2017.5787. Epub 2017 Feb 28.

DOI:10.3892/ol.2017.5787
PMID:28454446
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5403482/
Abstract

Colorectal cancer is one of the most common types of cancer worldwide. Previous studies have revealed that certain members of tripartite motif (TRIM) proteins are involved in carcin ogenesis regulation, but little is known about the function of TRIM68 in human colorectal cancer. To investigate the role of TRIM68 in colorectal cancer SW1116 and HCT116 cell lines, the present study conducted lentivirus-mediated knockdown against TRIM68 and demonstrated that depletion of TRIM68 notably inhibits colorectal cancer cell proliferation and colony formation ability. Cell cycle arrest in the G0/G1 phase and cycle accumulation in sub-G1 phase provided evidence that TRIM68 may participate in the regulation of colorectal cancer tumorigenesis. The results revealed the significant role of in regulating colorectal cancer cell mitosis and indicated that may be a promising therapeutic target.

摘要

结直肠癌是全球最常见的癌症类型之一。先前的研究表明，三联基序（TRIM）蛋白家族的某些成员参与致癌作用调控，但关于TRIM68在人类结直肠癌中的功能知之甚少。为了研究TRIM68在结直肠癌SW1116和HCT116细胞系中的作用，本研究进行了慢病毒介导的TRIM68敲低，并证明TRIM68的缺失显著抑制结直肠癌细胞增殖和集落形成能力。细胞周期停滞在G0/G1期以及亚G1期的周期积累提供了证据，表明TRIM68可能参与结直肠癌肿瘤发生的调控。结果揭示了 在调节结直肠癌细胞有丝分裂中的重要作用，并表明 可能是一个有前景的治疗靶点。 （注：原文中“ ”处内容缺失）

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/869a/5403482/80ff24ad4338/ol-13-04-2649-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/869a/5403482/dc3a749bff95/ol-13-04-2649-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/869a/5403482/820baf5e6165/ol-13-04-2649-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/869a/5403482/bb9570449fa0/ol-13-04-2649-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/869a/5403482/80ff24ad4338/ol-13-04-2649-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/869a/5403482/dc3a749bff95/ol-13-04-2649-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/869a/5403482/820baf5e6165/ol-13-04-2649-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/869a/5403482/bb9570449fa0/ol-13-04-2649-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/869a/5403482/80ff24ad4338/ol-13-04-2649-g03.jpg

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The transcriptional cofactor TRIM33 prevents apoptosis in B lymphoblastic leukemia by deactivating a single enhancer.转录辅因子TRIM33通过使单个增强子失活来防止B淋巴细胞白血病中的细胞凋亡。
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TRIM8 anti-proliferative action against chemo-resistant renal cell carcinoma.
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Front Genet. 2022 Jul 19;13:876325. doi: 10.3389/fgene.2022.876325. eCollection 2022.
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High-Intensity Aerobic Exercise Suppresses Cancer Growth by Regulating Skeletal Muscle-Derived Oncogenes and Tumor Suppressors.高强度有氧运动通过调节骨骼肌衍生的癌基因和肿瘤抑制因子来抑制癌症生长。
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Multifaceted Roles of TRIM Proteins in Colorectal Carcinoma.TRIM 蛋白在结直肠癌中的多效性作用。
Int J Mol Sci. 2020 Oct 13;21(20):7532. doi: 10.3390/ijms21207532.
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E3 Ubiquitin Ligase TRIM Proteins, Cell Cycle and Mitosis.E3 泛素连接酶 TRIM 蛋白、细胞周期和有丝分裂。
Cells. 2019 May 27;8(5):510. doi: 10.3390/cells8050510.
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