Shan Yuqiang, Kong Wencheng, Zhu Akao, Yu Panpan, Xie Qi, Zheng Sixin, Jin Huicheng
Pharmazie. 2018 Jan 2;73(1):42-48. doi: 10.1691/ph.2018.7721.
Long non-coding RNAs (lncRNAs) play key roles in cancers, yet their potential molecular mechanisms are not well understood. The objective of this study is to examine the expression, biological functions and mechanism of lncRNA CCAL in gastric cancer (GC).
MTT and Colony formation assay were used to detect cell proliferation and the colony formation ability of gastric cancer cells. Wound healing, Migration, and invasion assay were respectively used to explore the migration, and invasion in gastric cancer cell lines. Real-time polymerase chain reaction (RT-PCR) was performed to determine the expression level of CCAL. Western Blot was used to determine the expression of related proteins.
In the present study, we found that CCAL was upregulated in gastric cancer cell lines. Patients whose tumors had high CCAL expression had a shorter overall survival than patients whose tumors had low CCAL expression. Overexpression CCAL promoted the proliferation, migration and invasion of GC by regulating the expression of myc.
The present study reveals that CCAL is an oncogenic lncRNA that promotes the tumorigenesis and progression of GC.
长链非编码RNA（lncRNAs）在癌症中发挥关键作用，但其潜在分子机制尚未完全明确。本研究旨在探讨lncRNA CCAL在胃癌（GC）中的表达、生物学功能及机制。
采用MTT法和集落形成试验检测胃癌细胞的增殖及集落形成能力。分别采用伤口愈合试验、迁移试验和侵袭试验探究胃癌细胞系的迁移和侵袭能力。运用实时聚合酶链反应（RT-PCR）检测CCAL的表达水平。采用蛋白质免疫印迹法检测相关蛋白的表达。
在本研究中，我们发现CCAL在胃癌细胞系中表达上调。肿瘤CCAL高表达的患者总生存期短于肿瘤CCAL低表达的患者。CCAL过表达通过调节myc的表达促进胃癌的增殖、迁移和侵袭。
本研究揭示CCAL是一种致癌lncRNA，可促进胃癌的发生和进展。
