CCNB1

Official Full Name

cyclin B1

Organism

Homo sapiens

GeneID

891

Background

The protein encoded by this gene is a regulatory protein involved in mitosis. The gene product complexes with p34(cdc2) to form the maturation-promoting factor (MPF). The encoded protein is necessary for proper control of the G2/M transition phase of the cell cycle. [provided by RefSeq, Aug 2017]

Synonyms

CCNB;

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Detailed Information

Recent Research Progress

CCNB1, an important member of the cyclin family, is a key initiator of mitosis and a rigorous quality control step. It plays a key role in regulating and forming a complex with cyclin-dependent kinase 1 (CDK1), phosphorylating its substrate to promote the transition of the cell cycle from G2 phase to mitosis. More and more evidence suggests that CCNB1 is involved in checkpoint control, whose dysfunction is an early event in tumorigenesis, and its expression of dysregulation is observed in many different human cancers, including breast cancer, cervical cancer, lung cancer, esophageal squamous cell carcinoma, and melanoma. At the same time, there is evidence that inhibition of CCNB1 expression makes breast cancer cells more sensitive to the chemotherapy drug paclitaxel, and CCNB1 is an independent predictor of HBV-associated hepatocellular carcinoma recurrence.

CCNB1 and breast cancer

Breast cancer is the most common malignancy among women, 70% of which are estrogen receptor positive (ER⁺). Identification of effective prognostic biomarkers and targets are critical for the management of breast cancer. Studies have shown that CCNB1 has significant predictive power in long-term non-metastatic survival, disease-free survival, recurrence-free survival, and overall survival in patients with ER⁺ breast cancer, and CCNB1 is closely associated with hormone resistance. In addition, Gene Set Enrichment Analysis (GSEA) showed that its expression was positively correlated with overexpressed genes in endocrine therapy resistant samples. Ding et al. demonstrated the interaction between CCNB1 and several available anticancer drugs using the CCNB1-drug interaction network. In conclusion, CCNB1 is a biomarker for the monitoring of ER⁺ breast cancer prognosis and hormone therapy effects. It is also a promising target for developing new strategies to prevent or even reverse the resistance of hormone therapy. Moreover, CCNB1 expression may be helpful in monitoring hormone therapy and guiding personalized treatment. However, in vivo and in vitro experiments as well as multicenter randomized controlled clinical trials are still required prior to clinical application.

CCNB1 and colorectal cancer

The high morbidity and mortality of colorectal cancer poses a serious public health problem worldwide. Recent studies have shown that CCNB1 mRNA and protein levels were up-regulated in a subset of human colorectal tumors and positively correlated with Chk1 expression. Inhibition of Chk1 results in a significant decrease in cell proliferation and CCNB1 protein expression in colorectal cancer cells. Furthermore, down-regulation of CCNB1 impairs colorectal cancer proliferation in vitro and tumor growth in vivo. Specifically, inhibition of CCNB1 caused strong G2/M arrest in HCT116 and SW480 cells, interfering with the expression of cdc25c and CDK1. In addition, CCNB1 inhibition induces apoptosis in certain colorectal cancer cells. Taken together, these results indicate that CCNB1 is activated by Chk1, exerts its carcinogenic effects in colorectal cancer cells, and may play a key role in the development of novel therapeutic approaches for colorectal cancer.

CCNB1 and HCC

The transcription factor Forkhead box protein M1 (FOXM1) plays a key role in cancer development and progression, including human hepatocellular carcinoma (HCC). However, the regulatory role and potential mechanisms of FOXM1 remain limited. Na et al. found that high levels of FOXM1 and CCNB1 expression were closely associated with poor prognosis in patients with HCC. And FOXM1 and CCNB1 were simultaneously overexpressed in liver tumor tissues. At the mRNA and protein levels, knockdown of FOXM1 significantly inhibited the expression levels of CCNB1 in HCC cell lines. Mechanistic studies indicated that FOXM1 directly binds to the promoter region of CCNB1 and regulates the expression level of the CCNB1 gene at the transcriptional level. Furthermore, loss of function and rescue experiments indicated that CCNB1 is required for FOXM1-driven proliferation in HCC cells. The results of the study partially explain that the dysregulated expression of FOXM1 play an important role in the proliferation of human hepatocellular carcinoma cells through transcriptional activation of CCNB1 expression. And it also emphasizes that the FOXM1/CCNB1 axis may be a potential target for the treatment of HCC.

CCNB1 and bladder cancer

There is increasing evidence that the dysregulation of PBRM1 leads to tumorigenesis. However, little is known about the biological function of PBRM1 in the development or progression of bladder cancer. Li et al. found that PBRM1 was down-regulated in bladder cancer cell lines and tissues compared to normal cell lines and normal tissues. Furthermore, low PBRM1 expression was associated with shorter overall survival in bladder cancer patients. PBRM1 inhibits bladder cancer cell growth in vitro and tumorigenicity in vivo, and PBRM1 induces G2 cell arrest by inhibiting CCNB1. In conclusion, studies have shown that PBRM1 exerted a tumor suppressing role and induced cell cycle arrest in bladder cancer, which might partly be due to CCNB1.

In conclusion, CCNB1 is a highly conserved family of cyclins that are expressed in almost all tissues of the human body and play a key role in controlling the cell cycle in G2/M conversion. Therefore, an in-depth understanding of the underlying mechanisms of CCNB1 in cancer malignant behavior will help to further explore potential therapeutic strategies for controlling malignant diseases.

References:

Kun Ding, et al. CCNB1 is a prognostic biomarker for ER+ breast cancer. Medical Hypotheses, 2014, 83: 359–364
J. P. Pandey, et al. Higher levels of antibodies to the tumour-associated antigen cyclin B1 in cancer-free individuals than in patients with breast cancer. Clinical and Experimental Immunology, 2014, 178: 75–78
Sandeep Rajput, et al. Inhibition of cyclin dependent kinase 9 by dinaciclib suppresses cyclin B1 expression and tumor growth in triple negative breast cancer. Oncotarget, 2016, 7(35):56864-56875
Fang Yifeng, et al. Chk1-induced CCNB1 overexpression promotes cell proliferation and tumor growth in human colorectal cancer. Cancer Biology & Therapy, 2014, 15(9):1268–1279
Eivind VE, et al. Enrichment of nuclear S100A4 during G2/M in colorectal cancer cells: possible association with cyclin B1 and centrosomes, Clin Exp Metastasis, 2015, 32:755–767
Na Chai, et al. FOXM1 promotes proliferation in human hepatocellular carcinoma cells by transcriptional activation of CCNB1. Biochemical and Biophysical Research Communications, 2018, 500: 924e929
Li Huang, et al. PBRM1 suppresses bladder cancer by cyclin B1 induced cell cycle arrest. Oncotarget,2015,6(18): 16366-16378
Seon-Kyu Kim, et al. Expression Signature Defined by FOXM1−CCNB1 Activation Predicts Disease Recurrence in Non−Muscle-Invasive Bladder Cancer. American Association for Cancer Research, 2014, 20(12):3233–43.

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