scholarly journals Long non‑coding RNA MDC1‑AS inhibits human gastric cancer cell proliferation and metastasis through an MDC1‑dependent mechanism

2017 ◽  
Author(s):  
Yin Qin ◽  
Shutong Zhuang ◽  
Jianfeng Wen ◽  
Kai Zheng
Keyword(s):  
Gastric Cancer ◽  
Gastric Cancer Cell ◽  
Human Gastric Cancer ◽  
Cancer Cell Proliferation ◽  
Non Coding Rna ◽  
Proliferation And Metastasis ◽  
Gastric Cancer Cell Proliferation ◽  
Long Non Coding Rna ◽  
Cell Proliferation And Metastasis ◽  
Dependent Mechanism

scholarly journals Exosomal miR-122-5p inhibits tumorigenicity of gastric cancer by downregulating GIT1

2021 ◽  
Vol 36 (1) ◽  
pp. 36-46
Author(s):  
Yigang Jiao ◽  
Li Zhang ◽  
Jun Li ◽  
Yuqi He ◽  
Xin Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Gastric Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Proliferation And Metastasis ◽  
Gastric Cancer Cell Proliferation ◽  
Gastric Cancer Progression ◽  
Cell Proliferation And Metastasis

Background: microRNAs (miRNAs) are non-coding RNAs with important roles in the progression of human cancers, including gastric cancer. Exosomes are extracellular vesicles, which could transfer numerous noncoding RNAs, such as miRNAs. Here, in our study, we intended to investigate the role of exosomal miR-122-5p in gastric cancer progression. Methods: Exosomes were isolated utilizing commercial kit or ultracentrifugation. Biomarkers of exosomes or epithelia-mesenchymal transition (EMT) were monitored by western blot. Expression levels of miR-122-5p and G-protein-coupled receptor kinase interacting protein-1 ( GIT1) were evaluated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) or western blot. Cell proliferation and apoptosis were assessed by colony formation assay, methyl thiazolyl tetrazolium assay and flow cytometry. Cell metastasis was evaluated via Transwell assay. The interaction between miR-122-5p and GIT1 was validated by dual-luciferase reporter assay. Furthermore, tumor growth in vivo was detected by xenograft assay. Results: Exosomes were successfully isolated. MiR-122-5p was downregulated in exosomes derived from the serum of gastric cancer patients. Exosomal miR-122-5p could hinder gastric cancer cell proliferation and metastasis in vitro and tumor growth in vivo. Knockdown of GIT1 also inhibited gastric cancer cell proliferation and metastasis. Exosomal miR-122-5p targeted GIT1 to alter cellular behaviors of gastric cancer cells. Conclusion: Exosomal miR-122-5p suppressed gastric cancer progression by targeting GIT1.

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