scholarly journals Lnc RNA MALAT 1 increases the stemness of gastric cancer cells via enhancing SOX 2 mRNA stability

FEBS Open Bio ◽  
2019 ◽  
Vol 9 (7) ◽  
pp. 1212-1222 ◽  
Author(s):  
Yiwen Xiao ◽  
Jingjing Pan ◽  
Qian Geng ◽  
Ge Wang
2018 ◽  
Vol 108 ◽  
pp. 338-346 ◽  
Author(s):  
Hu Song ◽  
Yixin Xu ◽  
Linseng Shi ◽  
Teng Xu ◽  
Ruizhi Fan ◽  
...  

PLoS ONE ◽  
2019 ◽  
Vol 14 (11) ◽  
pp. e0225107
Author(s):  
Po-Chu Lee ◽  
Jui-Chung Chiang ◽  
Chih-Yu Chen ◽  
Yin-Chieh Chien ◽  
Wei-Min Chen ◽  
...  

2021 ◽  
Author(s):  
Chunmei Ji ◽  
Xu Zhang ◽  
Wentong Fang ◽  
Ling Meng ◽  
Xiaolong Wei ◽  
...  

Abstract BackgroundRNPC1, was reported to act as a tumor suppressor by binding and regulating the expression of the target genes in various cancers. However, the role of RNPC1 on the gastric cancer and the underly mechanisms were still unclear.MethodsGastric cancer cells were stably transfected with lentivirus. Proliferation, migration, invasion, cell cycle in vitro as well as tumorigenesis in vivo were performed to assess the role of RNPC1. Quantitative real-time PCR, western blot and immunohistochemistry were used to detect the relation between RNPC1 and Aurora kinase B (AURKB). RNA immunoprecipitation(RIP), RNA electrophoretic mobility shift assay (REMSA), dual-luciferase reporter assay were employed to identify the direct binding sites of RNPC1 with AURKB mRNA. CCK-8 assay conducted to confirm the function of AURKB in RNPC1-induced growth promotion. ResultsHigh RNPC1 expression was found in gastric cancer tissues and cell lines, associated with high TNM stage. RNPC1 overexpression could significantly promote the proliferation, migration, invasion of gastric cancer cells. Knockdown of RNPC1 could impede gastric cancer tumorigenesis in nude mice. AURKB expression was positively related with RNPC1. RNPC1 binded to the 3'-untranslated region (3'-UTR) of AURKB directly and enhanced AURKB mRNA stability. AURKB could reversed the proliferation induced by RNPC1 in gastric cancer cells. RNPC1 resulted in mitotic defects, aneuploidy and chromosomal instability in gastric cancer cells, as AURKB did. ConclusionRNPC1 acted as an oncogene in gastric cancer by influencing cell mitosis by regulating AURKB mRNA stability, which may provide a potential biomarker and therapeutic target for gastric cancer.


2001 ◽  
Vol 120 (5) ◽  
pp. A31-A31
Author(s):  
H KATAOKA ◽  
T JOH ◽  
T OHSHIMA ◽  
Y ITOH ◽  
K SENOO ◽  
...  

2001 ◽  
Vol 120 (5) ◽  
pp. A82-A82 ◽  
Author(s):  
S MAEDA ◽  
Y MITSUNO ◽  
Y HIRATA ◽  
M AKANUMA ◽  
H YOSHIDA ◽  
...  

Author(s):  
Kyung Hee Lee ◽  
Eun Young Choi ◽  
Min Kyoung Kim ◽  
Myung Soo Hyun ◽  
Jong Ryul Eun ◽  
...  

2019 ◽  
Author(s):  
Ling Ma ◽  
Zhangding Wang ◽  
Mengyan Xie ◽  
Weiyou Zhu ◽  
Fengming Yang ◽  
...  

Author(s):  
Qiong Luo ◽  
Suyun Zhang ◽  
Donghuan Zhang ◽  
Rui Feng ◽  
Nan Li ◽  
...  

Background: Gastric cancer(GC) is currently one of the major malignancies that threatens human lives and health. Anlotinib is a novel small-molecule that inhibits angiogenesis to exert anti-tumor effects. However, the function in gastric cancer is incompletely understood. Objective: The aim of the present study was to investigate the anti-tumor effects and molecular mechanisms of anlotinib combined with dihydroartemisinin (DHA) in SGC7901 gastric cancer cells. Method: Different concentrations of anlotinib and DHA were used to treat SGC7901 gastric cancer cells, after which cell proliferation was measured. Drug interactions of anlotinib and DHA were analyzed by the Chou-Talalay method with CompuSyn software. proliferation, apoptosis, invasion, migration, and angiogenesis were measured using the cell counting kit-8 (CCK8) assay, flow cytometry, Transwell invasion assays, scratch assays, and chicken chorioallantoic membrane (CAM) assays. proliferation-associated protein (Ki67), apoptosis-related protein (Bcl-2), and vascular endothelial growth factor A (VEGF-A) were quantified by Western bloting. Results: The combination of 2.5 μmol/L of anlotinib and 5 of μmol/L DHA was highly synergistic in inhibiting cell growth, significantly increased the apoptosis rate and suppressed obviously the invasion and migration capability and angiogenesis of gastric cancer cells. In addition, the expression levels of Ki67, Bcl-2, and VEGF-A, as well as angiogenesis, were significantly decreased in the Combination of drugs compared with in control and either drug alone. Conclusion: The combination of anlotinib and DHA showed synergistic antitumor activity, suggesting their potential in treating patients with gastric cancer.


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