Cordycepin induces apoptosis by caveolin-1-mediated JNK regulation of Foxo3a in human lung adenocarcinoma

Joo, Jong Cheon; Hwang, Jung Hoo; Jo, Eunbi; Kim, Young Rang; Kim, Dae Joon; Lee, Kyung Bok; Park, Soo Jung; Jang, Ik Soon

doi:10.18632/oncotarget.14661

Cited by 48 publications

(32 citation statements)

References 42 publications

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“…Cav-1 then elevates phosphorylated JNK (p-JNK) that can further prevent Foxo3a phosphorylation and enhance its nuclear translocation. In the nucleus, Foxo3a can increase the expression of Bax and caspase-3, then the cells exhibit reinforced apoptosis [151]. Jorunnamycin A is an extract from Xestospongia sp., which can suppress Cav-1 expression to inhibit EMT and survival in H460, H292 and H23 cells [152].…”

Section: Multiple Cav-1-targeted Agentsmentioning

confidence: 99%

Multifaceted Roles of Caveolin-1 in Lung Cancer: A New Investigation Focused on Tumor Occurrence, Development and Therapy

Shi

Lai

et al. 2020

Cancers

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Lung cancer is one of the most common and malignant cancers with extremely high morbidity and mortality in both males and females. Although traditional lung cancer treatments are fast progressing, there are still limitations. Caveolin-1 (Cav-1), a main component of caveolae, participates in multiple cellular events such as immune responses, endocytosis, membrane trafficking, cellular signaling and cancer progression. It has been found tightly associated with lung cancer cell proliferation, migration, apoptosis resistance and drug resistance. In addition to this, multiple bioactive molecules have been confirmed to target Cav-1 to carry on their anti-tumor functions in lung cancers. Cav-1 can also be a predictor for lung cancer patients’ prognosis. In this review, we have summarized the valuable research on Cav-1 and lung cancer in recent years and discussed the multifaceted roles of Cav-1 on lung cancer occurrence, development and therapy, hoping to provide new insights into lung cancer treatment.

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Section: Multiple Cav-1-targeted Agentsmentioning

confidence: 99%

Multifaceted Roles of Caveolin-1 in Lung Cancer: A New Investigation Focused on Tumor Occurrence, Development and Therapy

Shi

Lai

et al. 2020

Cancers

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“…We found that C. militaris reduced the viability and migration activities, indicative of its potential ability to mediate apoptosis. In addition, in our previous researches, we investigated the anticancer effect of cordycepin that is major compound in C. militaris on human lung, renal, and ovarian cancer cells [17][18][19][20][21]. However, the molecular mechanism underlying the inhibitory effects of C. militaris on tumor cell proliferation and metastasis remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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

Jang

Yang

et al. 2020

BMC Complement Med Ther

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148

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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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“…Cordycepin was employed as a radiosensitizer in breast cancer in a preclinical study (56). Although this study did not elucidate a mechanism of action, Cordycepin may induce caveolin-1 (Cav-1) expression (119). Cav-1 can suppress the NRF2-elicited effects by reducing manganese-dependent superoxide dismutase (MnSOD) expression, an important downstream target of the NRF2 pathway (86).…”

Section: Natural and Synthetic Inductors And Inhibitors Of Nrf2 Signamentioning

confidence: 95%

Nuclear Factor Erythroid 2-Related Factor 2 in Regulating Cancer Metabolism

Smolková

Mikó

Kovàcs

et al. 2020

Antioxidants & Redox Signaling

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Significance: Nuclear factor erythroid 2 (NFE2)-related factor 2 (NFE2L2, or NRF2) is a transcription factor predominantly affecting the expression of antioxidant genes. NRF2 plays a significant role in the control of redox balance, which is crucial in cancer cells. NRF2 activation regulates numerous cancer hallmarks, including metabolism, cancer stem cell characteristics, tumor aggressiveness, invasion, and metastasis formation. We review the molecular characteristics of the NRF2 pathway and discuss its interactions with the cancer hallmarks previously listed. Recent Advances: The noncanonical activation of NRF2 was recently discovered, and members of this pathway are involved in carcinogenesis. Further, cancer-related changes (e.g., metabolic flexibility) that support cancer progression were found to be redox-and NRF2 dependent. Critical Issues: NRF2 undergoes Janus-faced behavior in cancers. The pro-or antineoplastic effects of NRF2 are context dependent and essentially based on the specific molecular characteristics of the cancer in question. Therefore, systematic investigation of NRF2 signaling is necessary to clarify its role in cancer etiology. The biggest challenge in the NRF2 field is to determine which cancers can be targeted for better clinical outcomes. Further, large-scale genomic and transcriptomic studies are missing to correlate the clinical outcome with the activity of the NRF2 system. Future Directions: To exploit NRF2 in a clinical setting in the future, the druggable members of the NRF2 pathway should be identified. In addition, it will be important to study how the modulation of the NRF2 system interferes with cytostatic drugs and their combinations. Antioxid. Redox Signal. 00, 000-000.

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Cordycepin induces apoptosis by caveolin-1-mediated JNK regulation of Foxo3a in human lung adenocarcinoma

Cited by 48 publications

References 42 publications

Multifaceted Roles of Caveolin-1 in Lung Cancer: A New Investigation Focused on Tumor Occurrence, Development and Therapy

Multifaceted Roles of Caveolin-1 in Lung Cancer: A New Investigation Focused on Tumor Occurrence, Development and Therapy

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

Nuclear Factor Erythroid 2-Related Factor 2 in Regulating Cancer Metabolism

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