Pub. Date : 2019 Feb 11
PMID : 30741422
8 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | Nicotine induces cell survival and chemoresistance by stimulating Mcl-1 phosphorylation and its interaction with Bak in lung cancer. | Nicotine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 2 | Our previous data found that nicotine promotes cell survival in lung cancer by affecting the expression of antiapoptotic protein Mcl-1, suggesting that the Mcl-1 may be a therapeutic target for patients with lung cancer. | Nicotine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 3 | Our previous data found that nicotine promotes cell survival in lung cancer by affecting the expression of antiapoptotic protein Mcl-1, suggesting that the Mcl-1 may be a therapeutic target for patients with lung cancer. | Nicotine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 4 | In this study, we found that the effects of drug resistance on nicotine-induced lung cancer cell lines were shown to influence the phosphorylation of Mcl-1. | Nicotine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 5 | Moreover, nicotine induces Mcl-1 phosphorylation exclusively at the T163 site, which results in enhancement of the antiapoptotic activity of Mcl-1 and increased cell survival. | Nicotine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 6 | Moreover, nicotine induces Mcl-1 phosphorylation exclusively at the T163 site, which results in enhancement of the antiapoptotic activity of Mcl-1 and increased cell survival. | Nicotine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 7 | Meanwhile, nicotine can reduce the sensitivity of H1299 cells to CDDP via enhancement of the binding of Mcl-1 to Bak, which inhibits the proapoptotic effect of Bak and ultimately leads to increased survival and drug resistance of lung cancer cells. | Nicotine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |
| 8 | Thus, nicotine-induced cell survival and chemoresistance may occur in a mechanism by stimulating Mcl-1 phosphorylation and its interaction with Bak, which may contribute to improving the efficacy of chemotherapy in the treatment of human lung cancer. | Nicotine | MCL1 apoptosis regulator, BCL2 family member | Homo sapiens |