Long noncoding RNA NEAT1 regulates radio-sensitivity via microRNA-27b-3p in gastric cancer
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Cancer Cell International Open Access
PRIMARY RESEARCH
Long noncoding RNA NEAT1 regulates radio‑sensitivity via microRNA‑27b‑3p in gastric cancer Ying Jiang, Shan Jin, Shisheng Tan, Yingbo Xue and Xue Cao*
Abstract Background: Long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) exhibits an oncogenic role in multiple cancers, including gastric cancer (GC). But, the functions of NEAT1 in modulating radio-sensitivity of GC and its potential molecular mechanisms have not been totally elucidated. Methods: qRT-PCR was performed to detect the expressions of NEAT1 and microRNA-27b-3p (miR-27b-3p). Kaplan– Meier survival curves for NEAT1 expression in GC created using KM Plotter. Colony formation assay was used to determine the survival fraction. Cell apoptosis was evaluated by flow cytometry. Luciferase reporter assay was used to verify the relationship between miR-27b-3p and NEAT1. Results: NEAT1 was highly expressed while miR-27b-3p was downregulated in GC tissues and cells. NEAT1 was negatively correlated with that of miR-27b-3p and associated with poor overall survival. Moreover, NEAT1 and miR-27b-3p varied inversely after radiation in GC tissues and cells. Loss of NEAT1 or upregulation of miR-27b-3p increased the effect of radiation on cell survival fraction inhibition and apoptosis promotion. In addition, NEAT1 negatively regulated the expression of miR-27b-3p in GC cells. Interestingly, the depletion of miR-27b-3p dramatically attenuated the NEAT1 knockdown-mediated function in AGS and MKN-45 cells treated with radiation in vitro. Similarly, downregulation of NEAT1 enhanced the radiation-mediated inhibition of tumor growth, which was mitigated by decrease of miR-27b-3p. Conclusion: NEAT1 depletion enhanced radio-sensitivity of GC by negatively regulating miR-27b-3p in vitro and in vivo. Keywords: Gastric cancer, NEAT1, miR-27b-3p, Radio-sensitivity Background Gastric cancer (GC) is the most common malignant tumors in the digestive system and the leading cause of cancer mortality worldwide [1–3]. It has been reported that approximately 990,000 people are diagnosed with GC worldwide every year, of whom about 738,000 die from this disease [4]. Although researchers have made
*Correspondence: [email protected] Department of Oncology, The People’s Hospital of Guizhou, No. 83, Zhongshan East Road, Guiyang 550002, Guizhou, China
great progress in anti-cancer treatment during the last decades, the overall survival of GC is still low. Radiotherapy has been the primary method for GC [5, 6], whereas the radio-resistance is an obstacle of radiotherapy. Therefore, it has great significance to explore the exact mechanisms underlying the radiation response of GC. It is well documented that long noncoding RNAs (lncRNAs) are crucial in regulating cellular processes such as proliferation, metastasis, and apoptosis [7, 8]. Moreover, the exploration of lncRNAs in cancers has been reported [9]. For example, lncRNA Colorectal Neoplasia Differentially Expressed (CRNDE) is upregulated in colorectal
© The Author(s) 2020
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