Abstract
KIF26B is a member of the kinesin superfamily that is up-regulated in various tumors, including breast cancer (BC), which can promote tumor progression. This study aimed to investigate the potential function of KIF26B in BC, and the underlying mechanisms, focusing mainly on cell proliferation. KIF26B expression was examined in BC tissue samples obtained from 99 patients. Then, we performed MTS, EdU and flow cytometry assays to detect cell proliferation, and western blotting to measure the expression of cell cycle-related proteins in MDA-MB-231 and MDA-MB-468 cells following KIF26B knockdown. Promoter analysis was used to study the upstream regulatory mechanism of KIF26B. KIF26B was upregulated in BC tissues. High expression of KIF26B was associated with clinicopathological parameters, such as positive lymph node metastasis, higher tumor grade, and higher proliferative index in BC. Furthermore, knockdown of KIF26B expression inhibited MDA-MB-231 and MDA-MB-468 cell proliferation, arresting cells in the G1 phase of the cell cycle in vitro. Similarly, KIF26B silencing decreased the expression levels of Wnt, β-catenin, and cell cycle-related proteins such as c-Myc, cyclin D1, and cyclin-dependent kinase 4, while increasing the expression of p27. Moreover, ELK1 could bind to the core promoter region of KIF26B and activate its transcription. KIF26B acts as an oncogene in BC by regulating multiple proteins involved in the cell cycle. ELK1 activates KIF26B transcription.
Highlights
Breast cancer (BC) is one of most common malignant tumors and has become the second risk factor for cancer-related mortality in women worldwide
KIF26B is up-regulated in BC tissues and cell lines
We found that KIF26B was significantly up-regulated in ductal carcinoma in situ (DCIS) and invasive ductal carcinoma (IDC) compared with adjacent normal tissues (p
Summary
Breast cancer (BC) is one of most common malignant tumors and has become the second risk factor for cancer-related mortality in women worldwide. Metastasis and uncontrolled proliferation of tumor cells are two of the most important factors [1, 2]. Accumulating evidence demonstrates that KIF26B can regulate cytoskeleton-driven processes, such as cell migration, polarization, mitosis and adhesion and plays an important role in the development of the kidney and the nervous system [4,5,6]. More recent studies have suggested that KIF26B plays an important role in the oncogenesis or progression of many human cancer types [7, 8]. High KIF26B expression is strongly linked to poor prognosis in patients with BC or colorectal cancer [9,10,11]. The role of KIF26B in BC, especially the relationship between high KIF26B expression and cell proliferation, has rarely been reported
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