Evidence map›Paper›PMID 26303320›Full record

ArticleScientific reports2015

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

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

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Role of p38 MAPK Signalling in Testis Development and Male Fertility.Oxidative medicine and cellular longevity · 2022
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Anti-Cancer Effect of Cordycepin on FGF9-Induced Testicular Tumorigenesis.International journal of molecular sciences · 2020
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Bo-Syong PanInstitute of Basic Medical Sciences, College of Medicine, National Chen Kung University, Tainan, Taiwan, Republic of China.
Yang-Kao WangInstitute of Basic Medical Sciences, College of Medicine, National Chen Kung University, Tainan, Taiwan, Republic of China.
Meng-Shao LaiInstitute of Basic Medical Sciences, College of Medicine, National Chen Kung University, Tainan, Taiwan, Republic of China.
Yi-Fen MuDepartment of Cell Biology and Anatomy, College of Medicine, National Chen Kung University, Tainan, Taiwan, Republic of China.
Bu-Miin HuangInstitute of Basic Medical Sciences, College of Medicine, National Chen Kung University, Tainan, Taiwan, Republic of China.
National Cheng Kung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The p38 MAPKs play important roles in the regulation of balance between cell survival and cell death on the development of various cancers. However, the roles of p38 MAPKs regulating apoptotic effects on Leydig tumor cells remain unclear. In the present study, we showed that cordycepin (3'-deoxyadenosine) selectively induced apoptosis in MA-10 mouse Leydig tumor cells through regulating the p38 MAPK and PI3K/AKT signaling pathways. Cordycepin reduced viability in MA-10, TM4, and NT2/D1 cells, but not cause cell death of primary mouse Leydig cells on moderate concentration. Cordycepin increased reactive oxygen species (ROS) levels, which is associated with the induction of apoptosis as characterized by positive Annexin V binding, activation of caspase-3, and cleavage of PARP. Inhibition of p38 MAPKs activity by SB203580 significantly prevented cordycepin-induced apoptosis in MA-10 cells. Co-treatment with wortmannin or the autophagy inhibitor 3-methyladenine (3-MA) elevated levels of apoptosis in cordycepin-treated MA-10 cells. Moreover, cordycepin activated p53, p21 and TGFß; and downregulated CDK2. The antitumour activity of cordycepin-treated MA-10 cells was significantly distinct in severe combined immunodeficiency (SCID) mice in vivo. These results suggested that cordycein is a highly selective treatment to induce MA-10 cells apoptosis via p38 MAPKs signaling.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCell Line, TumorDeoxyadenosinesDose-Response Relationship, DrugGene Expression Regulation, NeoplasticLeydig Cell TumorMaleMAP Kinase Signaling SystemMiceMice, SCIDOncogene Protein v-aktPhosphatidylinositol 3-KinaseTreatment OutcomeAntineoplastic AgentscordycepinDeoxyadenosinesOncogene Protein v-aktPhosphatidylinositol 3-Kinase

Identifiers

PMID26303320
PMCPMC4548195
OpenAlexW1179856379

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.