Upregulated hsa_circRNA_100269 inhibits the growth and metastasis of gastric cancer through inactivating PI3K/Akt axis
Viability assay
MTT assay
DOI:
10.1371/journal.pone.0250603
Publication Date:
2021-04-26T19:09:45Z
AUTHORS (2)
ABSTRACT
The pathogenesis of GC involves the complex networking multiple signaling pathways; however, detailed mechanisms tumorigenesis remains largely unknown. Therefore, it is necessary to explore novel diagnostic/prognostic biomarkers for GC. In this study, levels hsa_circRNA_100269 in gastric cancer (GC) samples and cells were examined, its effects on biological functions elucidated. specimens/cell lines examined using RT-qPCR. Cell models with overexpression or knockdown generated lentiviral vectors. viability was determined by MTT assay; cell migratory/invasive activity evaluated wound healing/Transwell assay. cycle arrest apoptosis assessed flow cytometry; expression associated markers involved apoptosis, EMT PI3K/Akt RT-qPCR/immunoblotting. vivo study also performed knockout mice. Our findings revealed downregulation tissues compared non-cancerous control. Additionally, PI3K remarkably elevated tissues, where negatively correlated. Moreover, histology grade occurrence metastasis patients. addition, downregulated normal epithelial cells. Overexpressed notably inhibited proliferation, migration, invasion cells, whereas at G0/G1 phase promoted enhanced. hsa_circRNA_100269-regulated invasion, apoptosis. Knockdown induced tumor growth mouse model. summary, our indicated that reduced Furthermore, could suppress development inactivating pathway. More importantly, hsa_circRNA_100269/PI3K/Akt axis may be a therapeutic candidate treatment.
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