scholarly journals Role of transforming growth factor β1 in the inhibition of gastric cancer cell proliferation by melatonin in vitro and in vivo

2019 ◽  
Author(s):  
Hui Liu ◽  
Yu Zhu ◽  
Hui Zhu ◽  
Rong Cai ◽  
Kai‑Fang Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Gastric Cancer Cell ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Cancer Cell Proliferation ◽  
Gastric Cancer Cell Proliferation

scholarly journals Lentivirus-Mediated VEGF Knockdown Suppresses Gastric Cancer Cell Proliferation and Tumor Growth in vitro and in vivo

2020 ◽  
Vol Volume 13 ◽  
pp. 1331-1341 ◽  
Author(s):  
Jong-Hyung Park ◽  
Jin-Hee Seo ◽  
Hee-Yeon Jeon ◽  
Sun-Min Seo ◽  
Han-Kyul Lee ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Gastric Cancer Cell Proliferation

scholarly journals CDC27 Facilitates Gastric Cancer Cell Proliferation, Invasion and Metastasis via Twist-Induced Epithelial-Mesenchymal Transition

2018 ◽  
Vol 50 (2) ◽  
pp. 501-511 ◽  
Author(s):  
Yongfan Xin ◽  
Shili Ning ◽  
Liang Zhang ◽  
Ming Cui
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Gastric Cancer Cell ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Cell Proliferation ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
Gastric Cancer Cell Proliferation

Background/Aims: Lymph node metastasis is the primary cause of cancer-related death among patients with gastric cancer (GC), and cell division cycle 27 (CDC27) promotes the metastasis and epithelial-mesenchymal transition in many cancers. Till now, the mechanisms underlying CDC27-induced the epithelial-mesenchymal transition (EMT) of GC are still unclear. Methods: We analyzed the expression levels of CDC27 and EMT-related biomarkers using immunohistochemistry and Western blot in 60 cases of GC tissues, and then GC cells with CDC27 shRNAs or plasmids were subjected to in vitro and in vivo assays, including CCK-8, wound healing and transwell assays. Results: The CDC27 expression was obviously increased in GC tissues, and significantly correlates with EMT-related biomarkers, lymph node metastasis and poor 5-year overall survival. Additionally, in vitro and in vivo assays demonstrated that silencing of CDC27 expression effectively inhibited GC cell proliferation, invasion and metastasis. Conversely, CDC27 overexpression led to the opposite results. Finally, we demonstrated that Twist shRNA inhibited CDC27-meditated invasion and EMT of GC cells. Conclusion: CDC27 facilitates gastric cancer cell proliferation, invasion and metastasis via Twist-induced EMT; thus, this study offered a new therapy method for GC patients.

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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