Modulation of autophagy in exJSRV-env-transfected cells through the AktimTOR and MAPK signaling pathway
Modulation of autophagy in exJSRV-env-transfected cells through the AktimTOR and MAPK signaling pathway
复制标题
通过 AktimTOR 和 MAPK 信号通路调节 exJSRV-env 转染细胞的自噬
DOI：
10.1016/j.bbrc.2017.02.099
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发表时间：
2017
影响因子：
3.1
通讯作者：
Liu Shuying
中科院分区：
文献类型：
--
作者：
Sun Xiaolin;Du Fangyuan;Liu Shuying
The envelope (Env) ofJaagsiekte sheep retrovirus(JSRV) is an oncoprotein of ovine pulmonary adenocarcinoma (OPA). Autophagy is involved in different cancers, but how it is carcinogenic in JSRV Env is unclear. Modulation of autophagy in exJSRV-env-NM-transfected cells through the Akt/mTOR and MAPK signaling pathway was studied, and we observed strong positive labeling of p-Akt, p-mTOR, p-MEK1/2, p-ERK1/2, p-p38 and p-JNK in tumor cells and typical type II pneumocytes in naturally infected OPA lung tissues, which was co-aligned with JSRV-Env positive cells as shown by immunohistochemical and microscopic analysis. Akt/mTOR and MAPK pathways were activated in OPA lung and JSRV-Env transfected NIH 3T3 cells. Decreased Beclin1 and LC3 II/I suggested that autophagy was inhibited in OPA lung and JSRV-Env transfected NIH 3T3 cells. Beclin1 and LC3 II/I increased in JSRV-Env transfected NIH3T3 cells treated with mTOR inhibitor (rapamycin), ERK1/2 inhibitor (PD 98059), p38 inhibitor (SB 203580) and JNK inhibitor (SP 600125), suggesting that Akt/mTOR and MAPK pathways were responsible for JSRV-Env decreased autophagy. In conclusion, JSRV Env decreased autophagy in JSRV-Env transfected NIH3T3 cells through Akt/mTOR and MAPK pathways, in particular, JNK and p38 pathways.
