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Silencing of HAS2‐AS1 mediates PI3K/AKT signaling pathway to inhibit cell proliferation, migration, and invasion in glioma
Author(s) -
Zhao Zhenyi,
Liang Tiansong,
Feng Shijun
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28430
Subject(s) - glioma , cancer research , gene silencing , biology , pi3k/akt/mtor pathway , long non coding rna , antisense rna , hyaluronan synthase , signal transduction , gene expression , downregulation and upregulation , microbiology and biotechnology , gene , genetics
Hyaluronan synthase 2 (HAS2)‐AS1 (natural antisense transcript of HAS2) functions as oncogenic long noncoding RNA (lncRNA) in oral squamous cell carcinoma, breast cancer, and osteosarcoma. The role of HAS2‐AS1 in glioma remains unknown. In our research, HAS2‐AS1 expression was elevated in glioma tissues compared with normal brain tissues. Moreover, high levels of HAS2‐AS1 expression was observed in patients with glioma with high WHO grade (III‐IV) or large tumor size ( > 4 cm). The survival analysis from The Cancer Genome Atlas showed glioma cases with high HAS2‐AS1 expression that had shorter disease‐free survival time and overall survival time than those with low HAS2‐AS1 expression. In vitro studies suggested that knocking down HAS2‐AS1 expression inhibited glioma cell viability, migration, and invasion through phosphoinositide 3‐kinase/protein kinase B signaling pathway. In conclusion, HAS2‐AS1 may be considered as a predictor for clinical outcome and a potential therapeutic target in glioma.