Pub. Date : 2017 Jul 20
PMID : 28750889
6 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | Reciprocal activation of alpha5-nAChR and STAT3 in nicotine-induced human lung cancer cell proliferation. | Nicotine | signal transducer and activator of transcription 3 | Homo sapiens |
| 2 | Nicotine increased the levels of alpha5-nAChR mRNA and protein in NSCLC cell lines and activated the JAK2/STAT3 signaling cascade. | Nicotine | signal transducer and activator of transcription 3 | Homo sapiens |
| 3 | Nicotine-induced activation of JAK2/STAT3 signaling was inhibited by the silencing of alpha5-nAChR. | Nicotine | signal transducer and activator of transcription 3 | Homo sapiens |
| 4 | By silencing STAT3 expression, nicotine-induced upregulation of alpha5-nAChR was suppressed. | Nicotine | signal transducer and activator of transcription 3 | Homo sapiens |
| 5 | Downregulation of alpha5-nAChR and/or STAT3 expression inhibited nicotine-induced lung cancer cell proliferation. | Nicotine | signal transducer and activator of transcription 3 | Homo sapiens |
| 6 | These results suggest that there is a feedback loop between alpha5-nAChR and STAT3 that contributes to the nicotine-induced tumor cell proliferation, which indicates that alpha5-nAChR is an important therapeutic target involved in tobacco-associated lung carcinogenesis. | Nicotine | signal transducer and activator of transcription 3 | Homo sapiens |