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In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Bee venom inhibits growth of human cervical tumors in mice
Hye Lim Lee1, Sang Ho Park2, Tae Myoung Kim3
1College of Pharmacy and Medical Research Center, Heungduk, Cheongju, Chungbuk, Republic of Korea.
Abstract:
We studied whether bee venom (BV) inhibits cervical tumor growth through enhancement of death receptor (DR) expressions and inactivation of nuclear factor kappa B (NF-κB) in mice. In vivo study showed that BV (1 mg/kg) inhibited tumor growth. Similar inhibitory effects of BV on cancer growth in primary human cervical cancer cells were also found. BV (1-5 μg/ml) also inhibited the growth of cancer cells, Ca Ski and C33Aby the induction of apoptotic cell death in a dose dependent manner. Agreed with cancer cell growth inhibition, expression of death receptors; FAS, DR3 and DR6, and DR downstream pro-apoptotic proteins including caspase-3 and Bax was concomitantly increased, but the NF-κB activity and the expression of Bcl-2 were inhibited by treatment with BV in tumor mice, human cancer cell and human tumor samples as well as cultured cancer cells. In addition, deletion of FAS, DR3 and DR6 by small interfering RNA significantly reversed BV-induced cell growth inhibitory effects as well as NF-κB inactivation. These results suggest that BV inhibits cervical tumor growth through enhancement of FAS, DR3 and DR6 expression via inhibition of NF-κB pathway.
Insights
Bee venom (BV) effectively inhibits cervical tumor growth by increasing death receptor (DR) expression and decreasing nuclear factor kappa B (NF-κB) activity. This natural compound shows promise in cancer therapy.
Area of Science:
- Oncology
- Immunology
- Pharmacology
Background:
- Cervical cancer remains a significant global health challenge.
- Novel therapeutic strategies targeting cancer cell death pathways are needed.
- Bee venom (BV) possesses known anti-cancer properties requiring further investigation.
Purpose of the Study:
- To investigate the anti-cancer effects of bee venom (BV) on cervical tumor growth.
- To elucidate the molecular mechanisms involving death receptor (DR) expression and nuclear factor kappa B (NF-κB) signaling.
- To evaluate BV's potential as a therapeutic agent for cervical cancer.
Main Methods:
- In vivo studies using tumor-bearing mice treated with bee venom (BV).
- In vitro experiments on primary human cervical cancer cells and cell lines (Ca Ski, C33A).
- Analysis of death receptor (FAS, DR3, DR6) and apoptosis-related protein (caspase-3, Bax, Bcl-2) expression.
- Assessment of nuclear factor kappa B (NF-κB) activity.
- Gene silencing using small interfering RNA (siRNA) to validate target pathways.
Main Results:
- Bee venom (BV) significantly inhibited cervical tumor growth in vivo and in vitro.
- BV treatment dose-dependently induced apoptotic cell death in cancer cells.
- BV enhanced the expression of death receptors (FAS, DR3, DR6) and pro-apoptotic proteins (caspase-3, Bax).
- BV inhibited NF-κB activity and the expression of the anti-apoptotic protein Bcl-2.
- Silencing of death receptors reversed BV's inhibitory effects and NF-κB inactivation.
Conclusions:
- Bee venom (BV) demonstrates significant anti-cervical tumor growth activity.
- The mechanism involves the upregulation of death receptors (FAS, DR3, DR6) and induction of apoptosis.
- Inhibition of the NF-κB pathway is crucial for BV's anti-cancer effects, suggesting therapeutic potential.
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