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

Shuai Wu,Hongyan Jia,Rui Su,Anna Birková

doi:10.1155/2021/5511041

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 (p = 0.022∗) and pTNM stage (p = 0.021∗) of patients with TNBC. CCNB2 could promote the proliferation of TNBC cells in vitro 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.

Highlights

Triple-negative breast cancer (TNBC), which accounts for approximately 15% total incidence of breast cancer, is more aggressive than other types of breast cancers [1]
We investigated the expression levels of Cyclin B2 (CCNB2) in human breast cancer tissues according to the Cancer Genome Atlas (TCGA) database
Through the K-M survival analysis in TCGA database, we found that the expression of CCNB2 was obviously correlated with the disease-free survival rates of 2 sets of patients with breast cancer collected in different times (Figure 1(b), n = 803 and n = 963, respectively)

Summary

Introduction

Triple-negative breast cancer (TNBC), which accounts for approximately 15% total incidence of breast cancer, is more aggressive than other types of breast cancers [1]. TNBC was highly metastatic, suggesting that TNBC was prone to recurrence average 2 years after surgery [2]. The standard treatment methods for TNBC mainly included surgery, chemotherapy, radiation treatment, and combination treatment. Most TNBC patients still died within 5 years after therapy [3]. Targeted therapy has great advantages for the treatment of high-malignancy tumors, TNBC [4]. To combat this disease, more effective molecular targets are urgently needed

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Conclusion