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KMT2D 的下调抑制了胃癌的增殖并诱导了其凋亡。

Downregulation of KMT2D suppresses proliferation and induces apoptosis of gastric cancer.

机构信息

Department of Gastrointestinal Surgery, Guangdong Provincial Hospital of Chinese Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, 510120, Guangzhou, China.

Department of Digestive System, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.

出版信息

Biochem Biophys Res Commun. 2018 Sep 26;504(1):129-136. doi: 10.1016/j.bbrc.2018.08.143. Epub 2018 Sep 1.

DOI:10.1016/j.bbrc.2018.08.143
PMID:30177394
Abstract

PURPOSE

Histone lysine methyltransferase 2D (KMT2D/MLL2) is a known cancer-related protein; however, its function in gastric cancer (GC) remains uncharacterized. The present study sought to investigate the expression pattern and the role of KMT2D in GC.

METHODS

The expression of KMT2D were evaluated at mRNA and protein levels, while its clinico-pathological value were further explored. GC cells were transfected with KMT2D knockdown siRNAs or lentiviruses, and then detected by cell counting kit-8, plate clone formation, cell apoptosis, cycle, migration, invasion, and tumorigenesis assays.

RESULTS

Overexpression of KMT2D was observed in GC samples, and was strongly associated with poor survival. Depletion of KMT2D suppressed cell proliferation and induced apoptosis.

CONCLUSION

Our study demonstrated the upregulation of KMT2D in GC tissue, and KMT2D modulates proliferation and apoptosis in GC. Therefore, KMT2D might represent a novel oncogene for prognosis and optimal treatment of GC patients.

摘要

目的

组蛋白赖氨酸甲基转移酶 2D(KMT2D/MLL2)是一种已知的与癌症相关的蛋白质;然而,其在胃癌(GC)中的作用尚不清楚。本研究旨在探讨 KMT2D 在 GC 中的表达模式和作用。

方法

在 mRNA 和蛋白质水平评估 KMT2D 的表达,并进一步探讨其临床病理价值。用 KMT2D 敲低 siRNA 或慢病毒转染 GC 细胞,然后通过细胞计数试剂盒-8、平板克隆形成、细胞凋亡、细胞周期、迁移、侵袭和肿瘤发生实验进行检测。

结果

在 GC 样本中观察到 KMT2D 的过表达,并且与不良生存密切相关。KMT2D 的缺失抑制了细胞增殖并诱导了细胞凋亡。

结论

本研究表明 KMT2D 在 GC 组织中上调,KMT2D 调节 GC 中的增殖和凋亡。因此,KMT2D 可能代表 GC 患者预后和最佳治疗的新的癌基因。

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