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驱动蛋白家族成员 20B 通过促进细胞增殖来调节舌癌的进展。

Kinesin family member 20B regulates tongue cancer progression by promoting cell proliferation.

机构信息

Department of Stomatology, The Fifth Central Hospital of Tianjin, Tianjin Medical University, Tanggu, Tianjin 300450, P.R. China.

出版信息

Mol Med Rep. 2019 Mar;19(3):2202-2210. doi: 10.3892/mmr.2019.9851. Epub 2019 Jan 11.

DOI:10.3892/mmr.2019.9851
PMID:30664160
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6390006/
Abstract

Oral cancer refers to the malignant tumors that occur in the oral cavity, of which 80% are squamous cell carcinomas. The incidence of oral cancer accounts for ~5% of the incidence of systemic malignancies, with rapid progression, extensive infiltration and poor prognosis. In the present study, Kinesin family member (KIF)20B, a member of Kinesin‑6 family, was identified as a potential biomarker which could promote cancer progression. A total of 82 patients were recruited and KIF20B expression levels were investigated by immunohistochemistry, and were divided into high and low groups based on the median of KIF20B expression levels. The clinicopathological features and survival‑associated data of the two groups were analyzed and the results were provided as a table and by a Kaplan‑Meier plot, respectively. Additionally, KIF20B was successfully silenced in two tongue cancer cell lines, CAL‑27 and TCA‑8113. MTT and colony formation assay were performed to determine the changes of cell proliferation in knocked down‑KIF20B cell lines. In addition, proliferation‑associated proteins Ki67 and PCNA were investigated, by western blotting. In animal experiments, subcutaneous tumor formation was performed with control cells and cells with knocked down KIF20B, to determine the inhibitory effect of KIF20B in vivo. Firstly, it was found that there was significantly high expression levels of KIF20B in tongue cancer patients (P<0.05). Patients with high expression of KIF20B had poorer clinicopathological results including tumor differentiation level, lymph node metastasis and clinical stages. The overall survival and relapse‑free survival of high‑expression group were also poor. Secondly, after successful establishment of cells with knocked down KIF20B, this resulted in a notable reduction in cell proliferation in vitro. Subsequent western blotting further confirmed that Ki67 and PCNA expression levels had a significant decline. Finally, it was demonstrated that knocking down KIF20B could inhibit tumor volume growth in vivo. In conclusion, the high level of KIF20B in oral squamous cell carcinoma was significantly associated with poor clinicopathological features and survival. KIF20B might promote cancer development through enhancing cell proliferation in vitro, and might be a potential biomarker of oral squamous cell carcinoma.

摘要

口腔癌是指发生在口腔的恶性肿瘤,其中 80%为鳞状细胞癌。口腔癌的发病率约占全身恶性肿瘤的 5%,其具有进展迅速、广泛浸润和预后不良等特点。在本研究中,发现驱动蛋白家族成员(KIF)20B 是驱动蛋白-6 家族的一个成员,可作为促进癌症进展的潜在生物标志物。共招募了 82 名患者,通过免疫组织化学法检测 KIF20B 表达水平,并根据 KIF20B 表达水平的中位数将其分为高表达组和低表达组。分析两组的临床病理特征和生存相关数据,并分别以表格和 Kaplan-Meier 图的形式呈现结果。此外,成功沉默了两种舌癌细胞系 CAL-27 和 TCA-8113 中的 KIF20B。通过 MTT 和集落形成实验检测敲低 KIF20B 细胞系中细胞增殖的变化。此外,通过 Western blot 检测增殖相关蛋白 Ki67 和 PCNA。在动物实验中,用对照细胞和敲低 KIF20B 的细胞进行皮下肿瘤形成实验,以确定 KIF20B 在体内的抑制作用。首先,发现舌癌患者 KIF20B 的表达水平明显升高(P<0.05)。KIF20B 高表达的患者具有较差的临床病理结果,包括肿瘤分化水平、淋巴结转移和临床分期。高表达组的总生存率和无复发生存率也较差。其次,成功建立了敲低 KIF20B 的细胞系,导致体外细胞增殖明显减少。随后的 Western blot 进一步证实 Ki67 和 PCNA 的表达水平显著下降。最后,证明敲低 KIF20B 可抑制体内肿瘤体积的生长。总之,口腔鳞状细胞癌中 KIF20B 的高水平与不良的临床病理特征和生存显著相关。KIF20B 可能通过增强体外细胞增殖促进癌症发展,可能是口腔鳞状细胞癌的潜在生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c0d/6390006/c93a58451915/MMR-19-03-2202-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c0d/6390006/54f26c79d8d7/MMR-19-03-2202-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c0d/6390006/9dca5043a0ac/MMR-19-03-2202-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c0d/6390006/5e6161a1b58a/MMR-19-03-2202-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c0d/6390006/c93a58451915/MMR-19-03-2202-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c0d/6390006/54f26c79d8d7/MMR-19-03-2202-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c0d/6390006/9dca5043a0ac/MMR-19-03-2202-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c0d/6390006/5e6161a1b58a/MMR-19-03-2202-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c0d/6390006/c93a58451915/MMR-19-03-2202-g03.jpg

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