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Cited 3 time in webofscience Cited 8 time in scopus
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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 JungJang, Hyun-JinHwang, In-HuKim, Jung MinJo, EunbiLee, Min-GooJang, Ik-SoonJoo, Jong Cheon
Issue Date
Apr-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
Pages
6
Indexed
SCIE
SCOPUS
Journal Title
NATURAL PRODUCT COMMUNICATIONS
Volume
13
Number
4
Start Page
465
End Page
470
URI
https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/3683
ISSN
1934-578X
1555-9475
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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