The inhibitory effect of Cordycepin on the proliferation of cisplatin-resistant A549 lung cancer cells

Cho, Seong Hyeok; Kang, In‐Cheol

doi:10.1016/j.bbrc.2018.02.188

Cited by 19 publications

(8 citation statements)

References 26 publications

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“…However, there were controversial results on the effect of cordycepin on the distribution of cell cycle. Cho’s study reported that the proportion of the sub-G1 phases of cells treated with cordycepin and cells in control group were 15.9 ± 0.9% and 5.4% ± 0.9%, respectively, after 24 h of treatment, which indicated that cordycepin promoted apoptosis through accumulation of sub-G1 in A549 cisplatin-resistance lung cancer cells ( 27 ). And Lee’s research revealed that cordycepin enhanced sub-G1 and G2/M phase arrest of HT-29 cells at the concentration of 100 μM, while cordycepin at 200 and 400 μM enhanced G1 phase arrest ( 28 ).…”

Section: Discussionmentioning

confidence: 99%

Combination of Cordycepin and Apatinib Synergistically Inhibits NSCLC Cells by Down-Regulating VEGF/PI3K/Akt Signaling Pathway

et al. 2020

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Background: The application of apatinib is immensely limited by its acquired drug resistance. This research investigates whether cordycepin, a component from Cordyceps could synergize with apatinib to improve its anticancer effect on non-small cell lung cancer (NSCLC) cells. Methods: The NSCLC cell lines A549, PC9, and H1993, and human bronchial epithelial (HBE) cell line Bears-2B were used in this study. Cell counting kit 8, colony formation assays, wound healing assay, transwell assay, and flow cytometry analysis were performed to assess the cell viability, the migration ability, and invasion ability of the cells. Kyoto encyclopedia of genes and genomes (KEGG), western blotting and molecular docking was applied to analyze the possible pathways affected by cordycepin. Results: The combination of cordycepin and apatinib in a ratio of 5:1 synergistically reduced proliferation of NSCLC cells, inhibited cell migration and invasion, increased cell apoptosis by altering cell cycle in NSCLC A549 and PC9 cells. The VEGF/PI3K/Akt pathway was inhibited after treatment with cordycepin and apatinib. Conclusion: Our findings demonstrated that the combination of cordycepin and apatinib has synergistically anticancer effect on NSCLC cells by down-regulating VEGF/PI3K/Akt signaling pathway. This result indicated that cordycepin and apatinib could be a promising drug combination against NSCLC.

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Section: Discussionmentioning

confidence: 99%

Combination of Cordycepin and Apatinib Synergistically Inhibits NSCLC Cells by Down-Regulating VEGF/PI3K/Akt Signaling Pathway

et al. 2020

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“…Cordyceps militaris (L.) Link is a fungus belonging to the class Ascomycetes [11]. This fungus exhibits a wide spectrum of pharmacological activities, including anti-stress, antifatigue [12], antioxidant [13], antifungal, and anticancer [14]. The fruiting body of C. militaris contains various active components such as cordycepin, adenosine, polysaccharides, fatty acids, amino acids, and other chemicals [15].…”

Section: Introductionmentioning

confidence: 99%

Cordycepin Isolated from Cordyceps militaris: Its Newly Discovered Herbicidal Property and Potential Plant-Based Novel Alternative to Glyphosate

et al. 2019

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There is currently much interest in finding new phytochemicals among plants and fungi as nature-based alternatives to replace problematic herbicides such as glyphosate, which are preferentially used in agricultural production n. We discovered striking herbicidal potency in Cordyceps militaris (L.) and identified cordycepin as its principal plant growth inhibitor. Cordycepin obtained as an ethyl acetate extract was subjected to column chromatography and evaluated for its bioassay-guided phytotoxic capacity against Raphanus sativus (radish), showing a maximum inhibition on germination and growth of radish (IC50 = 0.052–0.078 mg/mL). Gas chromatography-mass spectrometry (GC-MS) (m/z: 251.2) and liquid chromatography-electrospray ionization-mass spectrometry (LC-ESI-MS) ([M + Na]+ m/z: 274.1; [M + H]+ m/z: 252.1) analyses confirmed cordycepin as the major component of the tested column fraction (55.38%). At 0.04 mg/mL, cordycepin showed 3.8–5.9- and 3.3–3.7-fold greater inhibition of the germination and growth of radish than benzoic acid (BA) and glyphosate, respectively. Compared with BA, isolated cordycepin reduced plant chlorophyll and carotenoid contents (2.0–9.5 -fold), while proline, total phenolic and total flavonoid contents were increased 1.2–1.8-fold. Finally, cordycepin promoted electrolyte leakage and malondialdehyde accumulation in radish aerial parts. Thus, cordycepin successfully isolated from Cordyceps militaris is a highly potent plant growth inhibitor with pending worldwide patent and may become a potential plant-based novel alternative to the disputed glyphosate.

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“…Cordycepin, also known as 3'deoxyadenosine, is known to be a primary bioactive component of C. militaris. The tumor-suppressive effect of cordycepin has been reported in various carcinoma cells [20][21][22].…”

Section: Discussionmentioning

confidence: 99%

Cordycepin Resensitizes T24R2, Cisplatin-resistant Human Bladder Cancer Cell, to Cisplatin by Inhibiting the AKT-mediated Ets-1 Activation

Kim¹,

Oh²,

Lee³

et al. 2020

Preprint

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Resistance of tumor cells to anticancer drugs is a major obstacle in tumor therapy. In this study, we investigated the mechanism of cordycepin-mediated resensitization to cisplatin inT24R2, a derived T24 cell line. Treatment with cordycepin or cisplatin (2 g/ml) alone could not induce cell death of T24R2, but combination treatment of these drugs significantly induced apoptosis of the cells through mitochondrial pathway including depolarization of mitochondrial membrane, decrease of anti-apoptotic proteins, Bcl-2, Bcl-xL, and Mcl-1, and increase of pro-apoptotic proteins, Bak and Bax. . High expression of MDR1 was the cause of cisplatin resistance in T24R2, and cordycepin significantly reduced MDR1 expression through inhibition of MDR1 promoter activity. MDR1 promoter activity was dependent on a transcription factor, Ets-1, in T24R2 cells. Although there is a correlation between MDR1 and Ets-1 expression in bladder cancer patients, active Ets-1, Thr-38 phosphorylated form (pThr-38), was critical to induce MDR1 expression. Cordycepin decreased pThr-38 Ets-1 level through inhibition of AKT, which reduced MDR1 transcription and induced the resensitization of T24R2 to cisplatin. The results suggest that cordycepin effectively resensitizes cisplatin-resistant bladder cancer cells to cisplatin, thus serving as a potential strategy for treatment of anti-cancer drug resistant patients.

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The inhibitory effect of Cordycepin on the proliferation of cisplatin-resistant A549 lung cancer cells

Cited by 19 publications

References 26 publications

Combination of Cordycepin and Apatinib Synergistically Inhibits NSCLC Cells by Down-Regulating VEGF/PI3K/Akt Signaling Pathway

Combination of Cordycepin and Apatinib Synergistically Inhibits NSCLC Cells by Down-Regulating VEGF/PI3K/Akt Signaling Pathway

Cordycepin Isolated from Cordyceps militaris: Its Newly Discovered Herbicidal Property and Potential Plant-Based Novel Alternative to Glyphosate

Cordycepin Resensitizes T24R2, Cisplatin-resistant Human Bladder Cancer Cell, to Cisplatin by Inhibiting the AKT-mediated Ets-1 Activation

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