BMP9 promotes autophagy and inhibits migration and invasion in breast cancer cells through the c-Myc/SNHG3/mTOR signaling axis

作者全名："Yu, Huomei; Chen, Yuanxiang; Lang, Lei; Liao, Deyu; Liu, Shiyan; Yu, Tao; Hu, Kai; Zhou, Lan; Zhang, Yan"

作者地址："[Yu, Huomei; Chen, Yuanxiang; Liao, Deyu; Liu, Shiyan; Yu, Tao; Hu, Kai; Zhou, Lan; Zhang, Yan] Chongqing Med Univ, Dept Lab Med, Key Lab Med Diagnost Minist Educ, Chongqing 400016, Peoples R China; [Lang, Lei] Chongqing Univ, Chongqing Univ Cent Hosp, Chongqing Emergency Med Ctr, Sch Med,Dept Clin Lab, Chongqing 400014, Peoples R China"

通信作者："Zhang, Y (通讯作者)，Chongqing Med Univ, Dept Lab Med, Key Lab Med Diagnost Minist Educ, Chongqing 400016, Peoples R China."

来源：TISSUE & CELL

ESI学科分类：MOLECULAR BIOLOGY & GENETICS

WOS号：WOS:000961740000001

JCR分区：Q1

影响因子：2.7

年份：2023

卷号：82

期号：　

开始页：　

结束页：　

文献类型：Article

关键词：Breast cancer; BMP9; Long non-coding RNA; Autophagy; Migration; Invasion

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 cMyc/SNHG3/mTOR signaling axis, which might offer a fresh perspective on BMP9's breast cancer-inhibiting properties."

基金机构："National Natural Science Foundation of China [81974449]; Basic Research and Frontier Exploration Project of Yuzhong District, Chongqing [20190135]"

基金资助正文："Acknowledgements The reported study was supported by the National Natural Science Foundation of China (No. 81974449) , Basic Research and Frontier Exploration Project of Yuzhong District, Chongqing (No. 20190135) ."