2. Apoptosis
  3. MDM-2/p53
  4. Safrole oxide

Safrole oxide is a p53 modulator that upregulates the expression of the p53 tumor suppressor protein, linking cell cycle arrest to the apoptotic process. Safrole oxide induces apoptosis in lung cancer cells without triggering necrosis. Safrole oxide can be used in lung cancer-related research.

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Safrole oxide

Safrole oxide Chemical Structure

CAS No. : 7470-44-2

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Safrole oxide Related Antibodies

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Description

Safrole oxide is a p53 modulator that upregulates the expression of the p53 tumor suppressor protein, linking cell cycle arrest to the apoptotic process. Safrole oxide induces apoptosis in lung cancer cells without triggering necrosis. Safrole oxide can be used in lung cancer-related research[1].

In Vitro

Safrole oxide (112.36-449.44 μM; 24-48 h) reduces the viability of A549 human lung cancer cells in a dose-dependent and time-dependent manner, with viability decreasing to 57.78% (24 h, 449.44 μM) and 12.62% (48 h, 449.44 μM) relative to control cells[1].
Safrole oxide (112.36-449.44 μM; 24 h) induces chromatin condensation and nuclear fragmentation, hallmarks of apoptosis, in A549 human lung cancer cells following 24 hours of treatment at concentrations from 112.36 to 449.44 μM[1].
Safrole oxide (449.44 μM; 48 h) does not induce necrosis in A549 human lung cancer cells after 48 hours of treatment, as indicated by unchanged LDH release relative to control cells[1].
Safrole oxide (224.72 μM; 24-48 h) blocks A549 human lung cancer cells completely at G1 phase and partly at G2-M phase over 24 to 48 hours of treatment, preventing cell cycle progression and driving cells toward apoptosis[1].
Safrole oxide (224.72 μM; 24 h) dramatically up-regulates P53 protein expression but does not affect H-Ras protein expression in A549 human lung cancer cells after 24 hours of treatment[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Safrole oxide Related Antibodies

Cell Viability Assay[1]

Cell Line: A549 human lung cancer cells
Concentration: 112.36 μM; 224.72 μM; 449.44 μM
Incubation Time: 24 h; 48 h
Result: Reduced cell viability to 85.39% (112.36 μM, 24 h), 78.85% (224.72 μM, 24 h) and 57.78% (449.44 μM, 24 h) relative to control.
Reduced cell viability to 68.73% (112.36 μM, 48 h, P < .01), 29.85% (224.72 μM, 48 h)

Apoptosis Analysis[1]

Cell Line: A549 human lung cancer cells
Concentration: 112.36 μM; 224.72 μM; 449.44 μM
Incubation Time: 24 h
Result: Initiated chromatin condensation and nuclear fragmentation in A549 cells.

Cell Cycle Analysis[1]

Cell Line: A549 human lung cancer cells
Concentration: 224.72 μM
Incubation Time: 24 h; 48 h
Result: Decreased S phase percentage to 16.78% and increased G2-M phase percentage to 14.28% after 24 h treatment, compared to control (S phase 20.03%, G2-M phase 7.30%).
Decreased S phase percentage to 0%, increased G0-G1 phase percentage to 74.73%, and increased G2-M phase percentage to 25.27% after 48 h treatment, compared to control (S phase 30.59%, G0-G1 phase 64.51%, G2-M phase 4.98%).

Immunofluorescence[1]

Cell Line: A549 human lung cancer cells
Concentration: 224.72 μM
Incubation Time: 24 h
Result: Increased relative fluorescence intensity of P53 protein from 31.14 to 51.73, indicating dramatic up-regulation.
Changed relative fluorescence intensity of H-Ras protein from 24.05 to 31.52, showing no significant difference.
Molecular Weight

178.18

Formula

C10H10O3
CAS No.
SMILES

C12=CC=C(CC3OC3)C=C1OCO2
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Safrole oxide Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Safrole oxide7470-44-2MDM-2/p53nuclear fragmentationlung cancer cellsH-Raschromatin condensationp53A549 human lung cancer cellscell cycle arrestapoptosisG2-M phaseG1 phaseInhibitorinhibitorinhibit

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