Related Experiment Video
Updated: Aug 19, 2026
Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons
Published on: April 24, 2021
[Molecular mechanisms of the protection of SNMC in HepG2 cell apoptosis]
Yan Wang1, Ying-Ji Ma, Bao-Shan Yang
1Department of Infectious Diseases, First Affiliated Hospital, Harbin Medical University, Harbin 150001, China.
Objective:
Apoptosis of the cells of liver cancer cell line HepG2 could be induced by TNF alpha and actinomycin D (Act D). In the current study, the molecular mechanism of the apoptosis protection of stronger neo-minophagen C (SNMC) to HepG2 cells was investigated.
Methods:
SNMC was added to the HepG2 cell culture medium when the cell concentration reached 0, 2, 20, 100, 200, 800 microg/ml 30 min before their apoptosis were inducted with TNF alpha and Act D. A flow cytometry assay was performed to detect the cell apoptosis rate; electromicroscopy was employed to visualize the subcellular structure after apoptosis. DNA ladder formation was checked with genomic DNA agarose electrophoresis. The expression pattern of apoptosis related protein Caspase-3, Bcl-2 and Bax was detected by Western blot.
Results:
After pretreatment with various concentrations of SNMC and 12 hours after treatment with TNF alpha and Act D, the HepG2 cell apoptosis rate and DNA ladder formation decreased dramatically when the SNMC concentration was higher in the media; the intracellular inactive form of Caspase-3 increased while the 17*10(3) active Caspase-3 decreased gradually. In addition, the expression of Bcl-2 increased and the expression of Bax decreased. Under the electromicroscope, the typical nucleolus condensation of HepG2 induced by TNF alpha and Act D was not seen among the 100 microg/ml SNMC treated cells.
Conclusion:
SNMC inhibits TNF alpha and Act D induced HepG2 cell apoptosis. This protective action may be regulated by intracellular apoptosis related factors.
Insights
Stronger neo-minophagen C (SNMC) protects HepG2 liver cancer cells from apoptosis induced by TNF alpha and actinomycin D. SNMC
Area of Science:
- Hepatocellular carcinoma research
- Cellular apoptosis mechanisms
- Drug-induced cell death studies
Context:
- Liver cancer cell line HepG2 is susceptible to apoptosis induced by tumor necrosis factor alpha (TNF α) and actinomycin D (Act D).
- Understanding the protective mechanisms against apoptosis is crucial for developing novel cancer therapies.
- Stronger neo-minophagen C (SNMC) is a potential therapeutic agent whose effects on apoptosis require elucidation.
Purpose:
- To investigate the molecular mechanisms underlying the apoptosis-protective effects of SNMC on HepG2 cells.
- To determine if SNMC can inhibit TNF α and Act D-induced apoptosis in liver cancer cells.
- To analyze the impact of SNMC on apoptosis-related proteins and cellular structures.
Summary:
- SNMC pretreatment significantly reduced the apoptosis rate and DNA ladder formation in HepG2 cells exposed to TNF α and Act D.
- SNMC modulated the expression of apoptosis-related proteins, increasing Bcl-2 and decreasing Bax, and altered Caspase-3 activity.
- Electromicroscopy revealed that SNMC prevented typical apoptotic morphological changes in HepG2 cells.
Impact:
- SNMC demonstrates a protective effect against TNF α and Act D-induced apoptosis in HepG2 cells.
- The findings suggest that SNMC's protective action is mediated by the regulation of intracellular apoptosis-related factors.
- This study provides a basis for further investigation of SNMC as a potential therapeutic agent in liver cancer treatment.
