自噬
PI3K/AKT/mTOR通路
生物
基因敲除
蛋白激酶B
液泡
长非编码RNA
癌症研究
细胞生物学
信号转导
核糖核酸
细胞质
基因
生物化学
细胞凋亡
作者
Huomei Yu,Yuanxiang Chen,Lei Lang,Deyu Liao,Shiyan Liu,Yu Tao,Kai Hu,Lan Zhou,Yan Zhang
出处
期刊:Tissue & Cell
[Elsevier BV]
日期:2023-03-17
卷期号:82: 102073-102073
被引量:5
标识
DOI:10.1016/j.tice.2023.102073
摘要
We previously reported that BMP9 inhibited breast cancer progression. However, the precise molecular mechanism is still unknown. Based on our RNA-sequencing (RNA-seq) results, BMP9 significantly down-regulated the expression of long non-coding RNA SNHG3. Exogenous BMP9 promoted autophagy and inhibited migration and invasion in MDA-MB-231 cells, which was effectively blunted by SNHG3 overexpression. Interestingly, SNHG3 was negatively connected with autophagy. Knockdown of SNHG3 induced autophagy by increasing the formation of autophagic vacuoles and thus inhibited the migration and invasion of MDA-MB-231 cells. Mechanically, BMP9-SNHG3 activated AMPK, AKT and mTOR signaling pathways to induce autophagy and inhibit migration and invasion. Meanwhile, BMP9 regulated SNHG3 transcription by suppressing c-Myc entry into the nucleus. In conclusion, BMP9 promotes autophagy and inhibits migration and invasion in breast cancer cells through the c-Myc/SNHG3/mTOR signaling axis, which might offer a fresh perspective on BMP9's breast cancer-inhibiting properties.
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