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Published on: January 11, 2019
[Mitochondrial mechanisms of antisense oligodeoxynucleotide Stat3 induced apoptosis in laryngeal carcinoma cell]
Haili Lü1, Quihang Zhang, Bo Yan
1Department of Otolaryngology-Head and Neck Surgery, Xuanwu Hospital, Capital University of Medical Science, Beijing 100053, China. lvhaili7823@gmail.com
Objective:
To investigate the changes of mitochondrion by transferring antisense oligodeoxynucleotide Stat3 into laryngeal carcinoma Hep-2 cell, for elucidating the mechanism of laryngeal carcinoma Hep-2 cell apoptosis, for developing more effective treatment for laryngeal cancer.
Method:
The designed Stat3 ASODN was transferred into laryngeal carcinoma Hep-2 cell by lipofection. Mitochondrion membrane potential, VDAC and Cyt-c were detected for determining the changes of mitochondrion.
Result:
MMP was fell, Cyt-c and VDAC were increased with the heighten concentration of ASODN.
Conclusion:
Mitochondria approach play an important role in the apoptosis mechanism of human Hep-2 cell by Stat3. This research elucidated the regulating mechanism of Hep-2 cell proliferation by Stat3, provided a new research focus for clinical therapy.
Insights
Transferring Stat3 antisense oligodeoxynucleotide into laryngeal cancer cells induced mitochondrial changes, promoting apoptosis. This finding offers new therapeutic strategies for laryngeal cancer treatment.
Area of Science:
- Molecular Biology
- Cell Biology
- Oncology
Context:
- Laryngeal carcinoma Hep-2 cells are a model for studying laryngeal cancer.
- Signal transducer and activator of transcription 3 (Stat3) is implicated in cancer cell proliferation and survival.
- Mitochondrial dysfunction is a key event in apoptosis.
Purpose:
- To investigate the effect of Stat3 antisense oligodeoxynucleotide (ASODN) on mitochondria in Hep-2 cells.
- To elucidate the role of Stat3 in laryngeal carcinoma cell apoptosis.
- To explore novel therapeutic targets for laryngeal cancer.
Summary:
- Stat3 ASODN was delivered into Hep-2 cells via lipofection.
- Mitochondrial membrane potential (MMP), voltage-dependent anion channel (VDAC), and cytochrome c (Cyt-c) were measured.
- Increased ASODN concentration led to decreased MMP and increased VDAC and Cyt-c levels.
Impact:
- Mitochondrial pathways are crucial in Stat3-mediated apoptosis of Hep-2 cells.
- This study clarifies Stat3's regulatory mechanism in Hep-2 cell proliferation.
- Provides a new research direction for clinical laryngeal cancer therapy.
