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2021 Targeted Therapies of Lung Cancer (TTLC) Meet ...
P10. Inhibitory Effect of Pemetrexed Disodium Hept ...
P10. Inhibitory Effect of Pemetrexed Disodium Heptahydrate on the Growth of KRAS-Dependent A549 Lung Cancer Cells
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Video Transcription
Inhibitory effect of Pimitrex disodium heptidate on the growth of CRAS-dependent A549 lung cancer cells. I do not have any relevant financial relationships to disclose. Figure 1 shows that Pimitrex-induced apoptosis evidenced by elevated expression of Clp-Caspas 9, Clp-Caspas 3, and Clp-PARP. Figure 2a reveals that Pimitrex increased the ROS level in a dose-dependent manner. The changes were accompanied by DNA fragmentation, which is represented by Figure 2b. Figure 3 indicates that increased pro-apoptotic Bax protein expression to induce loss of mitochondrial membrane potential. Figure 4 reveals that increased cellular sensors through increase of beta-galactosidase expression. Figure 5 shows that Pimitrex-induced cytotoxicity without inhibiting the RAS-REF-MEC-ERK signaling pathway but induced autophagy through activating MPK-M2 pathway. This slide indicates key outcomes of this study. Thank you very much.
Video Summary
The video discusses the inhibitory effect of Pimitrex disodium heptidate on the growth of CRAS-dependent A549 lung cancer cells. The figures presented in the video show that Pimitrex induces apoptosis, increases reactive oxygen species (ROS) levels, causes DNA fragmentation, leads to loss of mitochondrial membrane potential, and increases cellular sensors. Additionally, Pimitrex-induced cytotoxicity is explained, indicating that it activates the MPK-M2 pathway and induces autophagy without inhibiting the RAS-REF-MEC-ERK signaling pathway. These findings highlight the potential of Pimitrex as a treatment for lung cancer.
Asset Subtitle
Md Mohiddin
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Speaker
Md Mohiddin
Topic
Targeted Therapies - KRAS
Keywords
Pimitrex disodium heptidate
CRAS-dependent A549 lung cancer cells
apoptosis
reactive oxygen species (ROS)
mitochondrial membrane potential
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