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LncRNA-LOC101928316 contributes to gastric cancer progression through regulating PI3K-Akt-mTOR signaling pathway.

Chengyun Li | Geyu Liang | Sheng Yang | Jing Sui | Wenjuan Wu | Siyi Xu | Yancheng Ye | Bo Shen | Xiaomei Zhang | Yan Zhang
Cancer medicine | 2019

Long noncoding RNA (lncRNA) has played the important function in regulation of various biological processes and in diagnostic value has been widely appreciated. In the present study, we have found that LOC101928316 was significantly downregulated in gastric cancer (GC) tissues specimen, GC cell lines, and associated with the GC patients tumor, node, and metastasis (TNM) stage and degree of differentiation (P < 0.05). LOC101928316 overexpression can significantly inhibit SGC-7901 cell migration, invasion, and proliferation (P<0.05). LOC101928316 molecular mechanism investigates suggested that LOC101928316 can regulate PI3K-Akt-mTOR signaling pathway and change the GC development progression in vivo and in vitro. In vivo experiment also revealed that LOC101928316-Overexpression can inhibit the tumorigenicity of GC cells in tumor-burdened experimental nude mice (P < 0.05). LOC101928316 may function as anti-oncogene and also plays an important role in GC tumorigenesis. Collectively, our data provided the key role of LOC101928316 in the tumorigenesis of GC. In addition, the present study elucidates LOC101928316 potential regulatory network, which may help us to lead a better knowing of the pathogenesis of GC and probe the lncRNA as a novel biomarker to diagnosis and therapy for this malignant tumor.

Pubmed ID: 31207155

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