Bee venom inhibits growth of human cervical tumors in mice
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Hye Lim Lee1,*, Sang Ho Park2,*, Tae Myoung Kim3, Yu Yeon Jung1, Mi Hee Park1, Sang Hyun Oh1, Hye Seok Yun1, Hyung Ok Jun1, Hwan Soo Yoo1, Sang-Bae Han1, Ung Soo Lee4, Joo Hee Yoon5, Min Jong Song6, Jin Tae Hong1
1College of Pharmacy and Medical Research Center, Heungduk, Cheongju, Chungbuk, Republic of Korea
2Clinical Research Laboratory, Uijeonbu St. Mary's Hospital, The Catholic University of Korea College of Medicine, Uijeongbu, Republic of Korea
3College of Veterinary Medicine, Chungbuk National University, Heungduk, Cheongju, Chungbuk, Republic of Korea
4Department of Food Science & Technology, Korea National University of Transportation, Jeungpyeong, Republic of Korea
5Department of Obstetrics and Gynecology, St. Vincent's Hospital, College of Medicine, The Catholic University of Korea, Paldal-gu, Suwon, Gyeonggi-do, Republic of Korea
6Department of Obstetrics and Gynecology, Daejeon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Jung-gu, Daejeon, Republic of Korea
*These authors have contributed equally to this work
Jin Tae Hong e-mail: firstname.lastname@example.org
Min Jong Song e-mail: email@example.com
Keywords: bee venom, apoptosis, death receptors, NF-κB, cervical cancer
Received: November 27, 2014 Accepted: January 08, 2015 Published: January 23, 2015
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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