LncRNA CTD-3252C9.4 modulates pancreatic cancer cell survival and apoptosis through regulating IFI6 transcription

被引：18
作者：
Yin, Xin [2 ]
Yang, Jingyan [1 ]
Chen, Jintian [1 ]
Ni, Ruiqi [1 ]
Zhou, Yanhao [1 ]
Song, Hao [1 ]
Jin, Liang [1 ]
Tang, Tingting [3 ]
Pan, Yi [1 ]
机构：
[1] China Pharmaceut Univ, Sch Life Sci & Technol, State Key Lab Nat Med, Jiangsu Key Lab Druggabil Biopharmaceut, 24 Tongjiaxiang Ave, Nanjing, Jiangsu, Peoples R China
[2] Xuzhou Matern & Child Hlth Care Hosp, Ctr Genet Med, 46 Heping Rd, Xuzhou, Jiangsu, Peoples R China
[3] Xuzhou Med Univ, Canc Inst, 84 West Huaihai Rd, Xuzhou, Jiangsu, Peoples R China
来源：
CANCER CELL INTERNATIONAL | 2021年 / 21卷 / 01期
基金：
中国国家自然科学基金;
关键词：
Pancreatic cancer; Long noncoding RNA; Cell apoptosis; IFI6;
D O I：
10.1186/s12935-021-02142-0
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Background Pancreatic cancer (PC) is one of the most lethal cancer types with high degree of malignancy and poor prognosis. Recent studies have shown that long non-coding RNAs (lncRNAs) were associated with the initiation and progression of pancreatic cancer. In the current study, we have investigated the expression, biological function and mechanism of a lncRNA CTD-3252C9.4 in pancreatic cancer. Methods The expression of CTD-3252C9.4 in pancreatic cancer cells and tissues was measured by qRT-PCR. In vitro and in vivo functional experiments assays were implemented for identifying CTD-3252C9.4 function in pancreatic cancer. Molecular relationships among CTD-3252C9.4, IRF1 and IFI6 were investigated via luciferase reporter assay, pulldown assay and ChIP assays. Results CTD-3252C9.4 was found remarkably decreased in pancreatic cancer cells and tissues. Overexpression of CTD-3252C9.4 suppressed migration, invasion and proliferation, yet facilitated apoptosis of pancreatic cancer cells both in vitro and in vivo. Then, IFI6 was identified as a downstream target that could be down-regulated by CTD-3252C9.4 and IFI6 overexpression could counteract the effects of CTD-3252C9.4 upregulation on the survival and apoptosis of pancreatic cancer cells. Furthermore, mechanism experiments revealed that IRF1 was a transcriptional factor of IFI6 that can be blocked by CTD-3252C9.4 to inhibit IFI6 transcription. Conclusion Our data indicated that CTD-3252C9.4 could promote pancreatic cancer cell apoptosis and restrain cell growth via binding IRF1 and preventing the transcription of IFI6, which may become a potential therapeutic target for pancreatic cancer.
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页数：14
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