Anti-cancer effect and apoptosis induction of cordycepin through DR3 pathway in the human colonic cancer cell HT-29

Lee, Seung Yuan; Debnath, Trishna; Kim, Si-Kwan; Lim, Beong Ou

doi:10.1016/j.fct.2013.07.068

Cited by 83 publications

(46 citation statements)

References 53 publications

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“…It showed that some cells were damaged at the epithelia resulting in the release of the cytoplasm. Our data also confirmed the in vitro cytotoxic effect of cordycepin toward cancer cells, corresponding to that reported elsewhere [26][27][28].…”

Section: Organmicroanatomical Characteristic Of Tissuepercentage Of Csupporting

confidence: 80%

Toxicity evaluation of cordycepin and its delivery system for sustained in vitro anti-lung cancer activity

Aramwit¹,

Porasuphatana²,

Srichana³

et al. 2016

Nano Online

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Cite as: Pornanong Aramwit, Supatra Porasuphatana, Teerapol Srichana, Titpawan Nakpheng. Toxicity evaluation of cordycepin and its delivery system for sustained in vitro anti-lung cancer activity, nano Online (2016). DOI: https://doi.org/10.1515/nano.11671_2015.201Originally published in: Pornanong Aramwit, Supatra Porasuphatana, Teerapol Srichana, Titpawan Nakpheng. Toxicity evaluation of cordycepin and its delivery system for sustained in vitro anti-lung cancer activity, Nanoscale Research Letters. In the previous study, we have found that the cordycepin which was extracted from Cordyceps mycelia produced by growing Cordyceps militaris on the dead larva of Bombyx mori silkworms showed the anti-proliferative effect toward lung cancer cells without toxicity to non-cancer cells. In this work, the cordycepin was tested for its in vitro mutagenicity and in vivo toxicity. From the Ames test and subacute toxicity test using oral administration in a rat model, the cordycepin was proved to be a nonmutagenic and non-toxic compound. The hematology and blood chemistry as well as the microanatomical characteristic of the tissues of rats fed with cordycepin every day for consecutive 30 days were comparable to those of the normal ones. Then, the cordycepin was incorporated in gelatin type A (GA) and gelatin type B (GB) nanoparticles aimed to sustain its release and activity. The cordycepin incorporated in both GA and GB nanoparticles showed the sustained release profiles. GA nanoparticles could encapsulate cordycepin at higher encapsulation efficiency due to the attractive electrostatic interaction between the positive-charged GA and the negative-charged cordycepin. However, GA nanoparticles released cordycepin at the higher amount possibly because of the large surface area of small size nanoparticles. Comparing to GB nanoparticles, the higher amount of cordycepin released from GA nanoparticles showed the higher anti-proliferative and anti-migratory effects on A549 lung cancer cells. In conclusion, GA nanoparticles were suggested as a suitable carrier for the sustained release of cordycepin. The GA nanoparticles releasing cordycepin could be an effective and non-invasive material for the treatment of lung cancer cells.

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Section: Organmicroanatomical Characteristic Of Tissuepercentage Of Csupporting

confidence: 80%

Toxicity evaluation of cordycepin and its delivery system for sustained in vitro anti-lung cancer activity

Aramwit¹,

Porasuphatana²,

Srichana³

et al. 2016

Nano Online

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“…The role of DR3 in the development of some human malignancies has also been enlightened. DR3 expression was shown to be increased in human colon cancer cells treated with cordycepin, a deoxy form of adenosine, resulting in apoptosis induction [132]. A specific phenolic compound triggered apoptosis in human non-smallcell lung cancer (NSCLC) cells by increasing the expression of DR3 [133].…”

Section: Death Receptormentioning

confidence: 99%

Major apoptotic mechanisms and genes involved in apoptosis

et al. 2016

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As much as the cellular viability is important for the living organisms, the elimination of unnecessary or damaged cells has the opposite necessity for the maintenance of homeostasis in tissues, organs and the whole organism. Apoptosis, a type of cell death mechanism, is controlled by the interactions between several molecules and responsible for the elimination of unwanted cells from the body. Apoptosis can be triggered by intrinsically or extrinsically through death signals from the outside of the cell. Any abnormality in apoptosis process can cause various types of diseases from cancer to auto-immune diseases. Different gene families such as caspases, inhibitor of apoptosis proteins, B cell lymphoma (Bcl)-2 family of genes, tumor necrosis factor (TNF) receptor gene superfamily, or p53 gene are involved and/or collaborate in the process of apoptosis. In this review, we discuss the basic features of apoptosis and have focused on the gene families playing critical roles, activation/inactivation mechanisms, upstream/downstream effectors, and signaling pathways in apoptosis on the basis of cancer studies. In addition, novel apoptotic players such as miRNAs and sphingolipid family members in various kind of cancer are discussed.

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“…Previously, cordycepin has been revealed to induce apoptosis in a number of cancer cell lines, including breast (19), colon (20) and oral cancers (21), mouse leydig tumor (22), and oral squamous cell carcinoma (23). Cordycepin also induces autophagy in breast cancer cells (19) and has been used in a phase I study in combination with pentostatin to treat refractory acute lymphocytic or chronic myelogenous leukemia (Study ID, CDR0000065572) (24).…”

Section: Cordycepin Induces Apoptosis and Autophagy In Human Neuroblamentioning

confidence: 99%

Cordycepin induces apoptosis and autophagy in human neuroblastoma SK-N-SH and BE(2)-M17 cells

Li¹,

Li²,

Zhu³

et al. 2015

Oncology Letters

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Abstract. Cordycepin, also termed 3'-deoxyadenosine, is a derivative of the nucleoside adenosine that represents a potential novel class of anticancer drugs targeting the 3' untranslated region of RNAs. Cordycepin has been reported to induce apoptosis in certain cancer cell lines, but the effects of cordycepin on human neuroblastoma cells have not been studied. In the present study, an MTT assay revealed that cordycepin inhibits the viability of neuroblastoma SK-N-SH and BE(2)-M17 cells in a dose-dependent manner. In addition, cordycepin increases the early-apoptotic cell population of SK-N-SH cells, as determined by fluorescence-activated cell sorting analysis. The induction of apoptosis in neuroblastoma cells by cordycepin was further confirmed by western blotting, which revealed cleavage of caspase-3 and poly(adenosine diphosphate-ribose) polymerase 1 in the SK-N-SH and BE(2)-M17 cells. Cordycepin also induced the formation of a punctate pattern of light-chain 3 (LC3)-associated green fluorescence in the SK-N-SH cells transfected with a pEGFP-LC3 vector. Furthermore, western blotting revealed cleavage of LC3 A/B in cordycepin-treated neuroblastoma SK-N-SH cells. Taken together, the results indicate that cordycepin significantly increases apoptosis and autophagy in neuroblastoma cells, and may therefore be a drug candidate for neuroblastoma therapy, but requires additional evaluation.

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Anti-cancer effect and apoptosis induction of cordycepin through DR3 pathway in the human colonic cancer cell HT-29

Cited by 83 publications

References 53 publications

Toxicity evaluation of cordycepin and its delivery system for sustained in vitro anti-lung cancer activity

Toxicity evaluation of cordycepin and its delivery system for sustained in vitro anti-lung cancer activity

Major apoptotic mechanisms and genes involved in apoptosis

Cordycepin induces apoptosis and autophagy in human neuroblastoma SK-N-SH and BE(2)-M17 cells

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