Cordyceps militaris induces apoptosis in ovarian cancer cells through TNF-α/TNFR1-mediated inhibition of NF-κB phosphorylation View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2020-01-13

AUTHORS

Eunbi Jo, Hyun-Jin Jang, Kyeong Eun Yang, Min Su Jang, Yang Hoon Huh, Hwa-Seung Yoo, Jun Soo Park, Ik-Soon Jang, Soo Jung Park

ABSTRACT

BACKGROUND: Cordyceps militaris (L.) Fr. (C. militaris) exhibits pharmacological activities, including antitumor properties, through the regulation of the nuclear factor kappa B (NF-κB) signaling. Tumor Necrosis Factor (TNF) and TNF-α modulates cell survival and apoptosis through NF- κB signaling. However, the mechanism underlying its mode of action on the NF-κB pathway is unclear. METHODS: Here, we analyzed the effect of C. militaris extract (CME) on the proliferation of ovarian cancer cells by confirming viability, morphological changes, migration assay. Additionally, CME induced apoptosis was determined by apoptosis assay and apoptotic body formation under TEM. The mechanisms of CME were determined through microarray, immunoblotting and immunocytochemistry. RESULTS: CME reduced the viability of cells in a dose-dependent manner and induced morphological changes. We confirmed the decrease in the migration activity of SKOV-3 cells after treatment with CME and the consequent induction of apoptosis. Immunoblotting results showed that the CME-mediated upregulation of tumor necrosis factor receptor 1 (TNFR1) expression induced apoptosis of SKOV-3 cells via the serial activation of caspases. Moreover, CME negatively modulated NF-κB activation via TNFR expression, suggestive of the activation of the extrinsic apoptotic pathway. The binding of TNF-α to TNFR results in the disassociation of IκB from NF-κB and the subsequent translocation of the active NF-κB to the nucleus. CME clearly suppressed NF-κB translocation induced by interleukin (IL-1β) from the cytosol into the nucleus. The decrease in the expression levels of B cell lymphoma (Bcl)-xL and Bcl-2 led to a marked increase in cell apoptosis. CONCLUSION: These results suggest that C. militaris inhibited ovarian cancer cell proliferation, survival, and migration, possibly through the coordination between TNF-α/TNFR1 signaling and NF-κB activation. Taken together, our findings provide a new insight into a novel treatment strategy for ovarian cancer using C. militaris. More... »

PAGES

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Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s12906-019-2780-5

DOI

http://dx.doi.org/10.1186/s12906-019-2780-5

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1124060156

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/32020859


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28 schema:description BACKGROUND: Cordyceps militaris (L.) Fr. (C. militaris) exhibits pharmacological activities, including antitumor properties, through the regulation of the nuclear factor kappa B (NF-κB) signaling. Tumor Necrosis Factor (TNF) and TNF-α modulates cell survival and apoptosis through NF- κB signaling. However, the mechanism underlying its mode of action on the NF-κB pathway is unclear. METHODS: Here, we analyzed the effect of C. militaris extract (CME) on the proliferation of ovarian cancer cells by confirming viability, morphological changes, migration assay. Additionally, CME induced apoptosis was determined by apoptosis assay and apoptotic body formation under TEM. The mechanisms of CME were determined through microarray, immunoblotting and immunocytochemistry. RESULTS: CME reduced the viability of cells in a dose-dependent manner and induced morphological changes. We confirmed the decrease in the migration activity of SKOV-3 cells after treatment with CME and the consequent induction of apoptosis. Immunoblotting results showed that the CME-mediated upregulation of tumor necrosis factor receptor 1 (TNFR1) expression induced apoptosis of SKOV-3 cells via the serial activation of caspases. Moreover, CME negatively modulated NF-κB activation via TNFR expression, suggestive of the activation of the extrinsic apoptotic pathway. The binding of TNF-α to TNFR results in the disassociation of IκB from NF-κB and the subsequent translocation of the active NF-κB to the nucleus. CME clearly suppressed NF-κB translocation induced by interleukin (IL-1β) from the cytosol into the nucleus. The decrease in the expression levels of B cell lymphoma (Bcl)-xL and Bcl-2 led to a marked increase in cell apoptosis. CONCLUSION: These results suggest that C. militaris inhibited ovarian cancer cell proliferation, survival, and migration, possibly through the coordination between TNF-α/TNFR1 signaling and NF-κB activation. Taken together, our findings provide a new insight into a novel treatment strategy for ovarian cancer using C. militaris.
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35 schema:keywords B (NF-κB) signaling
36 Bcl-2
37 CME
38 Cordyceps militaris
39 Cordyceps militaris (L.) Fr
40 FR
41 Factor-Kappa B Signaling
42 IκB
43 NF-κB
44 NF-κB activation
45 NF-κB pathway
46 NF-κB phosphorylation
47 NF-κB signaling
48 NF-κB translocation
49 SKOV-3 cells
50 TEM
51 TNFR expression
52 TNFR results
53 TNFR1
54 XL
55 action
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57 active NF-κB
58 activity
59 antitumor properties
60 apoptosis
61 apoptosis assays
62 apoptotic body formation
63 apoptotic pathway
64 assays
65 binding
66 binding of TNF
67 body formation
68 cancer
69 cancer cell proliferation
70 cancer cells
71 caspases
72 cell apoptosis
73 cell lymphoma
74 cell proliferation
75 cell survival
76 cells
77 changes
78 consequent induction
79 coordination
80 cytosol
81 decrease
82 disassociation
83 disassociation of IκB
84 dose-dependent manner
85 effect
86 expression
87 expression induced apoptosis
88 expression levels
89 extract
90 extrinsic apoptotic pathway
91 factor receptor 1 (TNFR1) expression induced apoptosis
92 factors
93 findings
94 formation
95 immunoblotting
96 immunoblotting results
97 immunocytochemistry
98 increase
99 induced apoptosis
100 induction
101 inhibition
102 insights
103 interleukin
104 kappa B (NF-κB) signaling
105 levels
106 lymphoma
107 manner
108 marked increase
109 mechanism
110 mechanisms of CME
111 migration
112 migration activity
113 militaris
114 militaris (L.) Fr
115 militaris extract
116 mode
117 mode of action
118 modulates cell survival
119 morphological changes
120 necrosis factor
121 necrosis factor receptor 1 (TNFR1) expression induced apoptosis
122 new insights
123 novel treatment strategies
124 nuclear factor kappa B (NF-κB) signaling
125 nucleus
126 ovarian cancer
127 ovarian cancer cell proliferation
128 ovarian cancer cells
129 pathway
130 pharmacological activities
131 phosphorylation
132 proliferation
133 properties
134 receptor 1 (TNFR1) expression induced apoptosis
135 regulation
136 results
137 serial activation
138 signaling
139 strategies
140 subsequent translocation
141 survival
142 translocation
143 treatment
144 treatment strategies
145 tumor necrosis factor
146 tumor necrosis factor receptor 1 (TNFR1) expression induced apoptosis
147 upregulation
148 viability
149 viability of cells
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