MEK/ERK signalling has been identified as a key factor that terminates diapause in Sarcophaga crassipalpis and Bombyx mori. Paradoxically, high p‐MEK/p‐ERK signalling induces diapause in pupae of the moth Helicoverpa armigera; however, the regulatory mechanism is unknown. In the present study, we show that p‐MEK and p‐ERK are elevated in the brain of diapause‐destined pupae and suppression of MEK/ERK activity terminates diapause progress. Reactive oxygen species (ROS) activate MEK/ERK signalling, causing large‐scale phosphorylation of downstream proteins. The levels of ubiquitin‐conjugated proteins are also significantly reduced when ROS or p‐ERK level decreased. Moreover, terminated diapause progress by 20‐hydroxyecdysone injection significantly decreases p‐MEK, p‐ERK and phospho‐ribosomal S6 kinase levels, while phospho‐MAPK substrates and ubiquitin‐conjugated protein levels increase. Our data demonstrate that high MEK/ERK signalling mediated by ROS promotes diapause maintenance via increasing phosphorylation and degradation of downstream substrates. The results of this study may provide important information for understanding the regulatory mechanisms during insect diapause.
ABSTRACT. We investigated the effects of kinase insert domain receptor (KDR) gene silencing on the proliferation of A549 cells and their sensitivity to erlotinib. A KDR small interfering RNA (siRNA) sequence was designed and synthesized; then, it was transfected into A549 cells using Lipofectamine TM 2000. KDR mRNA and protein expression after KDR gene silencing was detected by reverse transcription polymerase chain reaction and western blotting; the A549 cell cycle was detected by flow cytometry. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and colony formation assay were performed to determine the sensitivity of A549 cells to erlotinib after KDR gene silencing. After 48h of KDR gene silencing, there was a significant decrease in KDR gene and protein expression (P < 0.05). The A549 cell cycle was arrested at the G0/G1 phase, and the number of cells in the S phase decreased; the difference was statistically significant (P < 0.05). In the KDR gene silencing group, the sensitivity of A549 cells to erlotinib was significantly enhanced (P < 0.05). KDR siRNA can significantly silence the KDR gene in A549 cells, inhibit the proliferation of A549 cells, and enhance their sensitivity to erlotinib.
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