Long non-coding RNA MEG3 attends to morphine-mediated autophagy of HT22 cells through modulating ERK pathway

Gao, Shuibo; Li, Enyao; Gao, Haixia

Previous studies reported that the expression of several lncRNAs were changed in the brains of addicted humans (Michelhaugh et al. 2011; Feng and Nestler 2013) . What's more, some lncRNAs have been demonstrated to contribute to neuroplasticity (Sartor et al. 2012; Bohnsack et al. 2019 ). These findings provide great motivation for studying the influences of lncRNAs on drug addiction. MEG3 has been proved to take part in the modulation of cell autophagy, especially in brain cells (Xu et al. 2018; Zhao et al. 2018) . Su et al. (2019) indicated that MEG3 might participate in the methamphetamine-mediated addiction in mice. In this study, we discovered that morphine exposure elevated the MEG3 expression in HT22 cells. Moreover, the silence of MEG3 relieved the morphine-stimulated HT22 cell autophagy through declining the Beclin-1 and LC3-II/ LC3-I expressions. Besides, we also discovered that the silence of MEG3 lowered the c-fos and p/t-ERK expressions in morphinetreated HT22 cells, but had no significant influence on OX1R and p/t-PKC expressions. Inhibitor of ERK pathway SCH772984 further promoted the influence of MEG3 silence on morphinecaused HT22 cell autophagy. Considering that c-fos and ERK pathway also have been found to join in the regulation of cell autophagy (Wu et al. 2018; Fung and Liu 2019) , the findings of our research suggested that up-regulation of MEG3 attended to the influence of morphine on HT22 cell autophagy might be achieved by elevating c-fos expression and promoting ERK pathway activation.