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Bee venom inhibits growth of human cervical tumors in mice.

Lee HL, Park SH, Kim TM, Jung YY, Park MH, Oh SH, Yun HS, Jun HO, Yoo HS, Han SB, Lee US, Yoon JH, Song MJ, Hong JT - Oncotarget (2015)

Bottom Line: Similar inhibitory effects of BV on cancer growth in primary human cervical cancer cells were also found.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.

View Article: PubMed Central - PubMed

Affiliation: College 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.

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Effect of BV on NF-κB activationNuclear extract from cervical cancer cells treated with BV (1, 2, and 5 μg/ml) for 2 hr was incubated in binding interaction of 32P-end-labeled oligonucleotide containing the NF-κB sequence. The present EMSA results are representatives of three experiments (A). The cells treated with BV (1, 2, and 5 μg/ml) for 2 hr was incubated and were lysed, cytosolic proteins were used to determine the expression of IκB, p-IκB (internal control) and nuclear proteins were used to determine the expression of p50, p65 and Histone-H1(internal control) in cervical cancer cells (B). Each band is representative for three experiments.
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Figure 7: Effect of BV on NF-κB activationNuclear extract from cervical cancer cells treated with BV (1, 2, and 5 μg/ml) for 2 hr was incubated in binding interaction of 32P-end-labeled oligonucleotide containing the NF-κB sequence. The present EMSA results are representatives of three experiments (A). The cells treated with BV (1, 2, and 5 μg/ml) for 2 hr was incubated and were lysed, cytosolic proteins were used to determine the expression of IκB, p-IκB (internal control) and nuclear proteins were used to determine the expression of p50, p65 and Histone-H1(internal control) in cervical cancer cells (B). Each band is representative for three experiments.

Mentions: NF-κB is significant in cervical cancer cell growth. To investigate whether BV inactivates NF-κB, we did EMSA for detecting DNA binding activity of NF-κB. We found that BV untreated cervical cancer cells showed highly constituted activation of NF-κB in both cervical cancer cells. However, the treatment of BV dose dependently inhibited DNA binding activity of NF-κB (Figure 7A). Agreed with the inhibition of NF-κB, cytosolic phosphorylation of IκB as well as the nucleus expression of p50 and p65 were inhibited by BV treatment in both cervical cancer cells (Figure 7B).


Bee venom inhibits growth of human cervical tumors in mice.

Lee HL, Park SH, Kim TM, Jung YY, Park MH, Oh SH, Yun HS, Jun HO, Yoo HS, Han SB, Lee US, Yoon JH, Song MJ, Hong JT - Oncotarget (2015)

Effect of BV on NF-κB activationNuclear extract from cervical cancer cells treated with BV (1, 2, and 5 μg/ml) for 2 hr was incubated in binding interaction of 32P-end-labeled oligonucleotide containing the NF-κB sequence. The present EMSA results are representatives of three experiments (A). The cells treated with BV (1, 2, and 5 μg/ml) for 2 hr was incubated and were lysed, cytosolic proteins were used to determine the expression of IκB, p-IκB (internal control) and nuclear proteins were used to determine the expression of p50, p65 and Histone-H1(internal control) in cervical cancer cells (B). Each band is representative for three experiments.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4466684&req=5

Figure 7: Effect of BV on NF-κB activationNuclear extract from cervical cancer cells treated with BV (1, 2, and 5 μg/ml) for 2 hr was incubated in binding interaction of 32P-end-labeled oligonucleotide containing the NF-κB sequence. The present EMSA results are representatives of three experiments (A). The cells treated with BV (1, 2, and 5 μg/ml) for 2 hr was incubated and were lysed, cytosolic proteins were used to determine the expression of IκB, p-IκB (internal control) and nuclear proteins were used to determine the expression of p50, p65 and Histone-H1(internal control) in cervical cancer cells (B). Each band is representative for three experiments.
Mentions: NF-κB is significant in cervical cancer cell growth. To investigate whether BV inactivates NF-κB, we did EMSA for detecting DNA binding activity of NF-κB. We found that BV untreated cervical cancer cells showed highly constituted activation of NF-κB in both cervical cancer cells. However, the treatment of BV dose dependently inhibited DNA binding activity of NF-κB (Figure 7A). Agreed with the inhibition of NF-κB, cytosolic phosphorylation of IκB as well as the nucleus expression of p50 and p65 were inhibited by BV treatment in both cervical cancer cells (Figure 7B).

Bottom Line: Similar inhibitory effects of BV on cancer growth in primary human cervical cancer cells were also found.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.

View Article: PubMed Central - PubMed

Affiliation: College 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.

Show MeSH
Related in: MedlinePlus