Cordyceps militaris Extract Inhibits the NF-KB pathway and Induces Apoptosis through MKK7-JNK Signaling Activation in TK-10 Human Renal Cell Carcinoma
- Authors
- Park, Soo Jung; Jang, Hyun-Jin; Hwang, In-Hu; Kim, Jung Min; Jo, Eunbi; Lee, Min-Goo; Jang, Ik-Soon; Joo, Jong Cheon
- Issue Date
- 4월-2018
- Publisher
- SAGE PUBLICATIONS INC
- Keywords
- Cordyceps militaris; Apoptosis; NF-KB; MKK7; JNK; TK-10.
- Citation
- NATURAL PRODUCT COMMUNICATIONS, v.13, no.4, pp.465 - 470
- Indexed
- SCIE
SCOPUS
- Journal Title
- NATURAL PRODUCT COMMUNICATIONS
- Volume
- 13
- Number
- 4
- Start Page
- 465
- End Page
- 470
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/76190
- ISSN
- 1934-578X
- Abstract
- The ubiquitous transcription factor, NF-KB, has been reported to inhibit apoptosis and induce drug resistance in cancer cells. Cordyceps militaris extract (CME) is involved in the regulation of the NF-KB signaling pathway. However, the detailed role of CME in the suppression of the NF-KB signaling pathway is unclear. We found that CME dose-dependently inhibited tumor necrosis factor-alpha (TNF-alpha)-induced NF-KB activation in TK-10 human renal cell carcinoma. CME prevented NF-KB from translocating to the nucleus, which resulted in the downregulation of GADD45B, upregulation of MKK7, and phosphorylation of JNK (p-JNK). The increased activation of Bax led to pronounced CME-induced apoptosis, which occurred through caspase-3. Furthermore, the siRNA-mediated knockdown of GADD45B inhibited MKK7 expression, whereas the siRNA-mediated inhibition of MKK7 downregulated p-JNK and the JNK inhibitor, SP600125, inhibited Bax expression. Thus, these results indicated that CME inhibited the activation of GADD45B via the inhibition of NF-KB activation, which upregulated the MKK7-JNK signaling pathway to induce apoptosis in TK-10 cells. Thus, this study reveals a novel anticancer function of CME.
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Collections - College of Medicine > Department of Medical Science > 1. Journal Articles
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