Cordycepin induced MA-10 mouse Leydig tumor cell apoptosis by regulating p38 MAPKs and PI3K/AKT signaling pathways

Pan, Bo; Wang, Yang Kao; Lai, Meng Shao; Mu, Yi Fen; Huang, Bu Miin

doi:10.1038/srep13372

Cited by 59 publications

(85 citation statements)

References 54 publications

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“…In this study, we postulated that NTS decreased SP1, and then decreased P27, activated MAPK pathway, finally inhibited cell apoptosis in EECs in vitro. In addition, many studied showed that PI3K also involved in the process of cell apoptosis [61], thus the PI3K protein level was also detected in this study, and the result showed that NTS decrease it in EECs. All these results suggested that NTS played very important and complex functions in the EECs apoptosis.…”

Section: Nts Promoted Eecs Proliferation and Inhibited Apoptosis In Vsupporting

confidence: 55%

WITHDRAWN: Endometrial epithelial cell apoptosis is inhibited via a ciR8073-miR181a-neurotensis pathway during embryo implantation

Zhang¹,

Liu²,

Liu³

et al. 2018

Oncotarget

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Development of receptive endometrium (RE) from pre-receptive endometrium (PE) is essential for embryo implantation, but the molecular mechanisms are not fully understood. In this study, lncRNA/circRNA-miRNA-mRNA networks were constructed to explore the functions of potential competing endogenous RNAs (ceRNA) during the development of RE in dairy goats. We observed that circRNA8073 (ciR8073) decreased levels of miR-181a by acting as a miRNA sponge. This effect indirectly increased expression of neurotensin in endometrial epithelial cells (EECs). Neurotensin in turn inhibited EEC apoptosis by increasing expression of BCL-2/BAX via the MAPK pathway, and also increased expression leukemia-inhibitory factor, cyclo-oxygenase 2, vascular endothelial growth factor A and homeobox A10. We have thus identified a ciR8073-miR181a-neurotensin pathway in the endometrium of dairy goats. Via this pathway, ciR8073 functions as a ceRNA that sequesters miR-181a, thereby protecting neurotensin transcripts from miR-181a-mediated suppression in EECs.

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Section: Nts Promoted Eecs Proliferation and Inhibited Apoptosis In Vsupporting

confidence: 55%

WITHDRAWN: Endometrial epithelial cell apoptosis is inhibited via a ciR8073-miR181a-neurotensis pathway during embryo implantation

Zhang¹,

Liu²,

Liu³

et al. 2018

Oncotarget

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show abstract

“…Cordycepin has been considered as an effective antioxidative agent with protective effects on respiratory system (14), nervous system (15), endocrine system (16), and tumor metastasis (12, 17, 18). Based on the characteristics of cordycepin, we hypothesized that cordycepin might also have effect on cartilage metabolism.…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that cordycepin possesses various biological functions, including antioxidant, hypolipidemic, and anti-inflammatory activities (10, 11). A recent study has confirmed that cordycepin may induce leydig tumor cells apoptosis via MAPK/P38 signaling (12). However, the role of cordycepin in cartilage reconstruction, especially in chondrocyte hypertrophy, remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Cordycepin inhibits chondrocyte hypertrophy of mesenchymal stem cells through PI3K/Bapx1 and Notch signaling pathway

Cao¹,

Dou

et al. 2016

BMB Reports

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Mesenchymal stem cells (MSCs) are widely used in cartilage tissue engineering to repair articular cartilage defects. However, hypertrophy of chondrocytes derived from MSCs might hinder the stabilization of hyaline cartilage. Thus, it is very important to find a suitable way to maintain the chondrogenic phenotype of chondrocytes. It has been reported that cordycepin has anti-inflammatory and anti-tumor functions. However, the role of cordycepin in chondrocyte hypertrophy remains unclear. Therefore, the objective of this study was to determine the effect of cordycepin on chondrogenesis and chondrocyte hypertrophy in MSCs and ATDC5 cells. Cordycepin upregulated chondrogenic markers including Sox9 and collagen type II while down-regulated hypertrophic markers including Runx2 and collagen type X. Further exploration showed that cordycepin promoted chondrogenesis through inhibiting Nrf2 while activating BMP signaling. Besides, cordycepin suppressed chondrocyte hypertrophy through PI3K/Bapx1 pathway and Notch signaling. Our results indicated cordycepin had the potential to maintain chondrocyte phenotype and reconstruct engineered cartilage. [BMB Reports 2016; 49(10): 548-553]

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“…However, it is rare on the investigation of antitumor effect of cordycepin on testicular tumor. Previously, we have reported that cordycepin could induce MA‐10 cell apoptosis by activating p38 MAPKs and inhibiting PI3K/AKT signaling pathways . However, the downstream signaling consequence of cordycepin‐induced p38 activation still needs to be further revealed.…”

Section: Introductionmentioning

confidence: 94%

Cordycepin‐induced unfolded protein response‐dependent cell death, and AKT/MAPK‐mediated drug resistance in mouse testicular tumor cells

et al. 2019

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Testicular cancer is the most commonly diagnosed cancer in men at 15‐44 years of age, and radical orchidectomy combined with chemotherapy is currently considered as the standard treatment. However, drugs resistance and side effects that impact the quality of life for patients with testicular cancer have not been markedly improved in recent decades. In this study, we characterized the pharmacological exacerbation of the unfolded protein response (UPR), which is an effective approach to kill testicular cancer cells, by carrying out a clustering analysis of mRNA expression profiles and the immunobloting examination of cordycepin‐treated MA‐10 cells. The UPR is executed in response to endoplasmic reticulum stress to complement by an apoptotic response if the defect cannot be resolved. Results showed that cordycepin significantly modulated FoxO/P15/P27, PERK‐eIF2α (apoptotic), and the IRE1‐XBP1 (adaptive) UPR pathways. Interestingly, a fraction of MA‐10 cells survived after cordycepin treatment, the AKT, LC3 I/II, and MAPK signaling pathways were highly induced in attached cells as compared to the suspended cells, illustrating the drug resistance to cordycepin via activating AKT and MAPK pathways in MA‐10 cells. In summary, PERK‐eIF2α signaling pathway is required for pro‐apoptotic UPR in MA‐10 cell death following cordycepin treatment, suggesting a potential therapeutic application in treating testicular cancer. However, activation of AKT and MAPK pathways could possibly result in drug resistance to cordycepin in MA‐10 cells.

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Cordycepin induced MA-10 mouse Leydig tumor cell apoptosis by regulating p38 MAPKs and PI3K/AKT signaling pathways

Cited by 59 publications

References 54 publications

WITHDRAWN: Endometrial epithelial cell apoptosis is inhibited via a ciR8073-miR181a-neurotensis pathway during embryo implantation

WITHDRAWN: Endometrial epithelial cell apoptosis is inhibited via a ciR8073-miR181a-neurotensis pathway during embryo implantation

Cordycepin inhibits chondrocyte hypertrophy of mesenchymal stem cells through PI3K/Bapx1 and Notch signaling pathway

Cordycepin‐induced unfolded protein response‐dependent cell death, and AKT/MAPK‐mediated drug resistance in mouse testicular tumor cells

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