Aim
To explore the potential activity of HOXA cluster antisense RNA 2 (HOXA-AS2), a long non-coding RNA (lncRNA), in epilepsy progression, as well as the mechanisms behind its activity. Material and
Conclusion
The current study suggested that targeting HOXA-AS2 could alleviate cellular damages in the epileptic model by regulating the miR-372-3p/STAT3 axis. Therefore, HOXA-AS2 may serve as a potential anti-epilepsy therapeutic target.
Material and methods
Kainic acid (KA) was used to treat rat astroglial CTX-TNA2 cells to establish a cellular model of epilepsy. Reverse transcription-quantitative PCR was conducted to examine the expression levels of HOXA-AS2, microRNA (miR)-372-3p and STAT3. Cell Counting Kit-8, flow cytometry and western blot assays were performed to analyze cell viability and apoptosis. The secretion levels of various inflammatory factors (IL-6, IL-1? and TNF-?) were identified by ELISA. To validate the functional interaction between HOXA-AS2/STAT3 and miR?372-3p, dual-luciferase reporter assay was performed.
Methods
Kainic acid (KA) was used to treat rat astroglial CTX-TNA2 cells to establish a cellular model of epilepsy. Reverse transcription-quantitative PCR was conducted to examine the expression levels of HOXA-AS2, microRNA (miR)-372-3p and STAT3. Cell Counting Kit-8, flow cytometry and western blot assays were performed to analyze cell viability and apoptosis. The secretion levels of various inflammatory factors (IL-6, IL-1? and TNF-?) were identified by ELISA. To validate the functional interaction between HOXA-AS2/STAT3 and miR?372-3p, dual-luciferase reporter assay was performed.
Results
The HOXA-AS2 and STAT3 expression levels were notably upregulated, whereas miR?372-3p was downregulated in KAtreated CTX-TNA2 cells. Silencing HOXA-AS2 or overexpressing miR-372-3p inhibited the secretion of inflammatory factors and apoptosis in KA-treated CTX-TNA2 cells. HOXA-AS2 negatively regulated miR?372-3p, and miR?372-3p targeted STAT3 mRNA. Suppression of miR-372-3p or overexpression of STAT3 abrogated the rescue effect of small interfering HOXA-AS2 in KA-treated CTX-TNA2 cells.