Pub. Date : 2020
PMID : 31956373
8 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | Nicotine Upregulates the Level of Mcl-1 through STAT3 in H1299 Cells. | Nicotine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 2 | Background: Nicotine contributes to development of human lung cancer and chemoresistance through activation of myeloid cell leukemia-1 (Mcl-1). | Nicotine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 3 | Background: Nicotine contributes to development of human lung cancer and chemoresistance through activation of myeloid cell leukemia-1 (Mcl-1). | Nicotine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 4 | Therefore, we examined the STAT3 cascade in nicotine regulation of Mcl-1 transcription in human lung cancer cells. | Nicotine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 5 | Methods: The effects of nicotine on the expression of STAT3 and Mcl-1 were determined using western blot. | Nicotine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 6 | Results: STAT3 was constitutively activated (i.e., tyrosine-phosphorylated, serine-phosphorylated and nuclear translocation), meanwhile the expression and transcriptional activity of Mcl-1 were up-regulated in lung cancer cells following treatment with nicotine. | Nicotine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 7 | Deleted mutagenesis of a putative STAT3 consensus binding sequence decreased Mcl-1 promoter activity and eliminated the increase of Mcl-1 promoter activity induced by nicotine. | Nicotine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 8 | Conclusions: We have demonstrated that nicotine induces up-regulation of Mcl-1 through STAT3, which process may be independent on JAKs and not only dependent on the phosphorylation of Y705. | Nicotine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |