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KMID : 1034820190150030335
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Molecular & Cellular Toxicology
2019 Volume.15 No. 3 p.335 ~ p.344
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Long non-coding RNA RP11-6O2.4 indicates poor prognosis and suppresses cell cycle progression through the p38-MAPK signaling pathway in gastric cancer
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Feng Yang
Fu Zhiming
Luo Yajun
Tan Wang
Liu Zilin
Ye Pengcheng
Lu Fei
Xiang Wanping
Tang Linghan
Yao Lin
Song Mengyun
Huang Qingmei
Liu Yilun
Xiao Jiangwei
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Abstract
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Backgrounds: The role of long non-coding RNAs (lncRNA) in gastric cancer (GC) has been highlighted in studies conducted over the past decade. However, the potential clinical value and the mechanisms of action of RP11?6O2.4 in GC have not been thoroughly elucidated to date. The specific aim of the present study was to assess RP11?6O2.4 and to explore its role in human GC.
Methods: Quantitative real-time polymerase chain reaction (qPCR) was performed to analyze the expression levels of RP11-6O2.4 in GC tissues, paired adjacent noncancerous tissues (ANTs) and GC cell lines. In addition, the correlation between RP11?6O2.4 expression and the clinical characteristics and prognosis of patients with GC was statistically analyzed. The effects of RP11-6O2.4 on the GC cell cycle transformation through the p38-MAPK signaling pathway were explored by flow cytometry, qPCR and Western blot analysis after treatment with SB203580, a p38MAPK specific inhibitor, in vitro.
Results: The expression levels of RP11-6O2.4 in GC tissues were significantly lower than the paired ANTs (P<0.05). In addition, RP11?6O2.4 expression was significantly lower in cases with older age, longer maximum tumor diameter, higher ASA grade and deeper invasive depth (P<0.05). RP11?6O2.4 expression was significantly higher in cases with well/middle differentiation than poor/no differentiation; higher in cases without lymph node metastasis than in lymph node metastasis; and higher in cases in stage I/II than in stage III/IV. An in vitro assay showed that RP11?6O2.4 induced G0/G1 phase cell cycle arrest, likely by regulating the p38-MAPK signaling pathway.
Conclusion: The above mentioned data suggested that RP11?6O2.4 was a tumor-suppressor gene in GC. RP11-6O2.4 might play an important role in the cell cycle transformation by regulating the p38-MAPK signaling pathway, thereby representing a specific biomarker and a potential molecular target for the treatment of GC.
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KEYWORD
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Long non-coding RNA, Gastric cancer, RP11-6O2.4, p38-MAPK
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