| General information | Literature | Expression | Regulation | Mutation | Homolog | Interaction |
Basic Information | |
|---|---|
Gene ID | 3569 |
Name | IL6 |
Synonymous | interleukin 6;IL6;interleukin 6 |
Definition | B-cell differentiation factor|B-cell stimulatory factor 2|BSF-2|CDF|CTL differentiation factor|IFN-beta-2|hybridoma growth factor|interferon beta-2|interferon, beta 2|interleukin BSF-2|interleukin-6 |
Position | 7p21 |
Gene type | protein-coding |
Title | Abstract |
| Cellular senescence and inflammation: a noteworthy link. | Although cellular senescence and inflammation have been indirectly associated, a direct connection was absent until recently, when two studies proved that senescence at a cellular level is directly linked to an interleukin (IL)-dependent inflammatory network. IL-6 and IL-8, two well-known proinflammatory cytokines, seem to play a central role in premature cellular senescence induction. Activation of the above-mentioned molecules and their receptors is necessary for the initiation of senescence while their deactivation ceases the process. Taking in consideration that atherosclerosis is an inflammatory process and cellular senescence is an emerging cardiovascular risk factor, these new data may be of great importance, especially for chronic kidney disease patients who suffer from increased cardiovascular disease morbidity. |
| DNA damage induces the IL-6/STAT3 signaling pathway, which has anti-senescence and growth-promoting functions in human tumors. | IL-6 is a multifunctional cytokine that is important for immune responses, cell survival, apoptosis, and proliferation. However, little is known about the correlation between the IL-6 signaling pathway and DNA damage in human tumors. The present study demonstrates the role of the IL-6/STAT3 signaling pathway in human tumor cells exposed to DNA damage. tumor cells exposed to DNA damage increase the expression and secretion of IL-6 and the phosphorylation of JAK1 and STAT3. The activation of the JAK1-STAT3 signaling pathway is inhibited by knockdown of gp130 or neutralization of soluble IL-6, implying that DNA damage induces the phosphorylation of JAK1 and STAT3 by autocrine IL-6. Interestingly, inhibition of the IL-6/STAT3 signaling pathway impairs the growth of tumor cells exposed to DNA damage and results in the induction of senescence. Therefore, the present study suggests that IL-6 inhibits senescence but promotes the survival and proliferation of tumor cells exposed to DNA damage through the activation of the JAK1-STAT3 signaling pathway. |