Department of Oncology, The First Hospital of Lanzhou University, Lanzhou 730000, Gansu Province, People's Republic of China; The First Clinical Medical College of Lanzhou University, Lanzhou 730000, Gansu Province, People's Republic of China.
Department of Oncology, The First Hospital of Lanzhou University, Lanzhou 730000, Gansu Province, People's Republic of China; The Second Clinical Medical College of Lanzhou University, Lanzhou 730030, Gansu Province, People's Republic of China.
Pathol Res Pract. 2019 May;215(5):988-994. doi: 10.1016/j.prp.2019.02.005. Epub 2019 Feb 16.
Recent studies have shown that Chondroitin polymerizing factor (CHPF) is abnormally expressed in malignant tumors, however, the expression of CHPF in lung adenocarcinoma (LUAD) has not been reported. In this study, the relationship of CHPF and LUAD will be explored.
Differential genes present in LUAD were screened by bioinformatics analysis. The expression status of CHPF in LUAD tissues and cell lines were deteced by Western blotting or Real-time Quantitative Polymerase Chain Reaction Detecting System (qPCR), and the relationship between CHPF and prognosis of LUAD patients was analyzed. CHPF was effectively silenced in LUAD cell lines by lentivirus- mediated methods. The effect of CHPF on proliferation, cell cycle progression and apoptosis of cancer cells was assessed. We further determined the role of CHPF in tumor growth in vivo by using xenograft LUAD tumor models. Western blotting assay was performed to assess the expression changes of MAPK signaling pathway.
We found that CHPF is highly expressed in LUAD tissues and cell lines. In vitro experiments, CHPF knockdown in LUAD cells can effectively inhibit proliferation and promote apoptosis of cancer cell. In vivo experiment, tumor growth was markedly inhibited by CHPF knockdown in the xenograft model of LUAD. Notably, CHPF also could promote tumor progression by regulating MAPK pathway.
CHPF can promote the proliferation and antiapoptosis of LUAD cells, which is promising to become a potential target for LUAD treatment.
最近的研究表明，软骨素聚合因子（CHPF）在恶性肿瘤中异常表达，然而，CHPF 在肺腺癌（LUAD）中的表达尚未报道。本研究旨在探讨 CHPF 与 LUAD 的关系。
通过生物信息学分析筛选 LUAD 中的差异基因。采用 Western blot 或实时定量聚合酶链反应检测系统（qPCR）检测 LUAD 组织和细胞系中 CHPF 的表达状态，并分析 CHPF 与 LUAD 患者预后的关系。采用慢病毒介导的方法有效沉默 LUAD 细胞系中的 CHPF。评估 CHPF 对癌细胞增殖、细胞周期进程和凋亡的影响。进一步通过 LUAD 肿瘤异种移植模型确定 CHPF 在体内肿瘤生长中的作用。采用 Western blot 检测 MAPK 信号通路的表达变化。
我们发现 CHPF 在 LUAD 组织和细胞系中高表达。体外实验中，CHPF 敲低可有效抑制 LUAD 细胞的增殖并促进癌细胞凋亡。体内实验中，CHPF 敲低明显抑制了 LUAD 肿瘤异种移植模型中的肿瘤生长。值得注意的是，CHPF 还可以通过调节 MAPK 通路促进肿瘤进展。
CHPF 可促进 LUAD 细胞的增殖和抗凋亡，有望成为 LUAD 治疗的潜在靶点。
