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细胞周期蛋白 B2(CCNB2)刺激三阴性乳腺癌(TNBC)细胞的增殖。

Cyclin B2 (CCNB2) Stimulates the Proliferation of Triple-Negative Breast Cancer (TNBC) Cells and .

机构信息

Department of Mammary Gland, The First Hospital of Shanxi Medical University, Taiyuan 030001, China.

Department of Critical Care Medicine, The Second Hospital of Shanxi Medical University, Taiyuan 030001, China.

出版信息

Dis Markers. 2021 Jul 26;2021:5511041. doi: 10.1155/2021/5511041. eCollection 2021.

DOI:10.1155/2021/5511041
PMID:34354775
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8331305/
Abstract

Triple-negative breast cancer (TNBC) is the most aggressive type of breast cancer. Currently, targeting therapy makes great advances for the treatment of TNBC, whereas more effective therapeutic targets are urgently needed. Cyclin B2 (CCNB2), which belongs to B-type cyclins, is known as a cell cycle regulator. CCNB2 is synthesized at G1 phase in cancer cells and downregulated at anaphase. The defects of CCNB2 led to the abnormal cell cycle and tumorigenesis. Though there are wide effects of CCNB2 on multiple types of tumors, the potential role of CCNB2 in TNBC progression is still unclear. Herein, we found that CCNB2 was highly expressed in human TNBC tissues and correlated with the prognosis and clinical pathological features including tumor size ( = 0.022) and pTNM stage ( = 0.021) of patients with TNBC. CCNB2 could promote the proliferation of TNBC cells and in mice. Our findings therefore confirmed the involvement of CCNB2 in TNBC progression and provided the evidence that CCNB2 could serve as a promising molecular target of TNBC.

摘要

三阴性乳腺癌(TNBC)是最具侵袭性的乳腺癌类型。目前,靶向治疗在 TNBC 的治疗方面取得了重大进展,但仍迫切需要更有效的治疗靶点。细胞周期素 B2(CCNB2)属于 B 型细胞周期素,是一种细胞周期调节剂。在癌细胞中,CCNB2 在 G1 期合成,并在后期下调。CCNB2 的缺陷导致细胞周期异常和肿瘤发生。尽管 CCNB2 对多种类型的肿瘤有广泛的影响,但 CCNB2 在 TNBC 进展中的潜在作用仍不清楚。在这里,我们发现 CCNB2 在人 TNBC 组织中高表达,与患者的预后和临床病理特征(包括肿瘤大小( = 0.022)和 pTNM 分期( = 0.021))相关。CCNB2 可以促进 TNBC 细胞的增殖。因此,我们的研究结果证实了 CCNB2 在 TNBC 进展中的作用,并提供了 CCNB2 可以作为 TNBC 有前途的分子靶点的证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55be/8331305/9c357840f2c3/DM2021-5511041.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55be/8331305/2db6e317d542/DM2021-5511041.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55be/8331305/80da15c377ca/DM2021-5511041.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55be/8331305/c8c553b43662/DM2021-5511041.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55be/8331305/619f32729919/DM2021-5511041.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55be/8331305/9c357840f2c3/DM2021-5511041.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55be/8331305/2db6e317d542/DM2021-5511041.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55be/8331305/80da15c377ca/DM2021-5511041.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55be/8331305/c8c553b43662/DM2021-5511041.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55be/8331305/619f32729919/DM2021-5511041.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55be/8331305/9c357840f2c3/DM2021-5511041.005.jpg

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