scholarly journals LPS-induced CXCR7 expression promotes gastric Cancer proliferation and migration via the TLR4/MD-2 pathway

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Nan Li ◽  
Huanbai Xu ◽  
Yurong Ou ◽  
Zhenzhong Feng ◽  
Qiong Zhang ◽  
...  
2019 ◽  
Vol 34 (4) ◽  
pp. 364-372 ◽  
Author(s):  
Zhigang Liu ◽  
Yun Lü ◽  
Qiuyu Jiang ◽  
Yang Yang ◽  
Chengxue Dang ◽  
...  

Purpose: miR-491 functions as a tumor suppressor in several types of cancer. However, its function and mechanism in gastric cancer proliferation and metastasis have not been well defined. The aim of this study was to explore the role and regulatory mechanism of miR-491 in cell proliferation and migration in gastric cancer. Methods: Quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) was used to detect the expression pattern of miR-491 in gastric cancer tissues. miR-491 overexpression vector, miR-491 inhibitor, and siHMGA2 were used; and MTT, wound healing, and transwell assays were employed to examine proliferation and migration for BGC-823 cells. A dual-luciferase reporter gene was used to measure the target relationship between miR-491 and HMGA2. Results: Most gastric cancer patients exhibit decreased miR-491 expression. miR-491 overexpression inhibited cell proliferation and migration, whereas miR-491 inhibitor treatment produced the opposite effect. Mechanistically, HMGA2 was identified as a direct target of miR-491. Moreover, HMGA2 knockdown inhibited cell proliferation and migration, which was similar to the effect of miR-491 overexpression. HMGA2 was decreased after transfection of the miR-491 vector and increased after transfection of the miR-491 inhibitor. Conclusion: Our results suggest that miR-491 suppressed cell proliferation and cell motility in gastric cancer by targeting HMGA2. Silencing HMGA2 produced a similar effect to miR-491 overexpression on cell proliferation and migration. miR-491/HMGA2 signaling may be a potential therapeutic target for gastric cancer patients with decreased miR-491 expression.


2019 ◽  
Vol 120 (8) ◽  
pp. 14107-14115 ◽  
Author(s):  
Mingming Zhang ◽  
Pei Liu ◽  
Famei Xu ◽  
Yuanlong He ◽  
Xiangjun Xie ◽  
...  

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Haithm Mousa ◽  
Menglang Yuan ◽  
Xinsheng Zhang ◽  
Xiaomeng Li ◽  
Abdullah Shopit ◽  
...  

2018 ◽  
Vol 120 (5) ◽  
pp. 7527-7538 ◽  
Author(s):  
Lianjun Ma ◽  
Xiaorui Chen ◽  
Chang Li ◽  
Rongjie Cheng ◽  
Zhuo Gao ◽  
...  

Life Sciences ◽  
2021 ◽  
Vol 276 ◽  
pp. 119436
Author(s):  
Keshav Raj Paudel ◽  
Ridhima Wadhwa ◽  
Xin Nee Tew ◽  
Natalie Jia Xin Lau ◽  
Thiagarajan Madheswaran ◽  
...  

2021 ◽  
Vol 53 (4) ◽  
pp. 454-462
Author(s):  
Ting Li ◽  
Xiaomin Zuo ◽  
Xiangling Meng

Abstract Circular RNAs (circRNAs) play either oncogenic or tumor suppressive roles in gastric cancer (GC). A previous study demonstrated that circ_002059, a typical circRNA, was downregulated in GC tissues. However, the role and mechanism of circ_002059 in GC development are still unknown. In this study, the levels of circ_002059, miR-182, and metastasis suppressor-1 (MTSS1) were examined by real-time quantitative polymerase chain reaction and western blot analysis. Cell proliferation and migration were evaluated by MTT assay and Transwell migration assay, respectively. The interactions between miR-182 and circ_002059 or MTSS1 were analyzed by dual-luciferase reporter assay. A GC xenograft model was established to validate the role of circ_002059 in GC progression in vivo. Overexpression of circ_002059 significantly inhibited, whereas knockdown of circ_002059 notably facilitated, cell proliferation and migration in GC cells. MTSS1 was found to be a direct target of miR-182 and circ_002059 upregulated MTSS1 expression by competitively sponging miR-182. Transfection with miR-182 mimic and MTSS1 silencing abated the inhibitory effect of circ_002059 on GC progression. Circ_002059 inhibited GC cell xenograft tumor growth by regulating miR-182 and MTSS1 expression. Collectively, Circ_002059 inhibited GC cell proliferation and migration in vitro and xenograft tumor growth in mice, by regulating the miR-182/MTSS1 axis.


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