Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.22.62 (caspase-9)
 7,507 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The responses of insect cells to starvation and the characteristics of cell death after the depletion of nutrients remain largely unknown. In the present study, we investigated autophagy, apoptosis and necrosis in two Lepidoptera insect cell lines in response to amino acid starvation. Our data demonstrated that starvation induced a significant increase in autophagy in Spodoptera litura SL-ZSU-1 cells, and cell apoptosis followed autophagy after starvation of more than 48h. However, at an early stage of starvation, inhibition of autophagy with 3-MA rapidly triggered apoptosis of SL-ZSU-1 cells, suggesting autophagy inhibits cell apoptosis. By contrast, Bombyx mori SPC Bm36 cells died by a non-apoptotic pathway if the starvation was prolonged for more than 48 h. At the early stage of starvation, inhibition of autophagy with 3-MA did not trigger apoptosis in Bm36 cells, but resulted in necrotic-like cell death. Under starvation pressure, autophagy in SL-ZSU-1 cells was much more active than in Bm36 cells. The activity of caspase-9-like in apoptotic SL-ZSU-1 cells also was much higher than in apoptotic Bm36 cells. RT-PCR analyses revealed that transcriptional levels of saposin-like (Bm109) and Atg6 were undetectable in Bm36 cells, but expression level of saposin-like in SL-ZSU-1 was high. Expression of Atg6 in SL-ZSU-1 cells was not analyzed because its sequence was unknown. These data indicate that autophagy prevents Lepidoptera insect cells from death at an early stage of starvation, but prolonged starvation results in cell death. The pathways of cell death might be dependent on the abundance of caspase-9-like, saposin-like and Atg6.
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PMID:Responses of two insect cell lines to starvation: autophagy prevents them from undergoing apoptosis and necrosis, respectively. 2133 11

Four suberoylanilide hydroxamic acid (SAHA) derivatives (N34, N4I, N4B, N24) were designed and synthesized on the basis of our previous studies on N25. Assays for anti-proliferative activity and histone deacetylase (HDAC) activity were performed against human lung cancer (SPC-A-1, LTEP-a-2, NCI-H1650) and normal lung cells (MRC-5), which were compared with those of SAHA. Molecular docking was used to theoretically confirm the receptor-binding ability of N34. Ultimately, N34 was validated as the best HDAC inhibitor candidate. Furthermore, the effects of N34 on the levels of apoptosis- and autophagy-associated proteins caspase-3, caspase-9, Bcl-2 and Beclin-1 in SPC-A-1 cells were evaluated. N34 exerted more evident effects on human lung cancer than the other three SAHA derivatives did.
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PMID:Screening Novel SAHA Derivatives as Anti-lung Carcinoma Agents: Synthesis, Biological Evaluation, Docking Studies and Further Mechanism Research between Apoptosis and Autophagy. 2611 11