Evidence map›Paper›PMID 33067427›Full record

ArticleCell death & disease2020

Cordycepin enhances the chemosensitivity of esophageal cancer cells to cisplatin by inducing the activation of AMPK and suppressing the AKT signaling pathway.

Ying Gao, Dan-Lei Chen, Mi Zhou, Zhou-San Zheng, Mei-Fang He, Sheng Huang, Xiao-Zhong Liao, Jia-Xing Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Transposon engineering ofEngineering in life sciences · 2026
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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

8 authors at 4 institutions in 1 country.

Ying GaoDepartment of Oncology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Dan-Lei ChenDepartment of Oncology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Mi ZhouDepartment of Oncology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Zhou-San ZhengDepartment of Oncology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Mei-Fang HeDepartment of Oncology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Sheng HuangDepartment of Orthopaedics, the First Affiliated Hospital of Nanchang University, 330006, Nanchang, China. hus163@163.com.
Xiao-Zhong LiaoDepartment of Oncology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China. liaoxzh3@mail2.sysu.edu.cn.
Jia-Xing ZhangDepartment of Oncology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510080, China. zhangjx25@mail.sysu.edu.cn.
Sun Yat-sen University · CNThe First Affiliated Hospital, Sun Yat-sen University · CNFirst Affiliated Hospital of Guangzhou University of Chinese Medicine · CNNanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although cisplatin (cDDP), is a first-line chemotherapy drug for esophageal cancer, it still has the potential to develop drug resistance and side effects. There is increasing evidence that cordycepin can work synergistically with other chemotherapy drugs. Therefore, we investigated whether combination therapy of cordycepin and cDDP may enhance the therapeutic effect of cDDP. We performed a series of functional tests to study the effect of medical treatment on esophageal cancer cells. We then used GO analysis to examine the pathways affected by treatment with cordycepin and cDDP. Next, we observed changes in the abundance of the selected pathway proteins. The in vivo animal model supported the results of the in vitro experiments. Co-treatment with cordycepin and cDDP inhibited cell growth, migration, and metastasis, as well as induced apoptosis. Cordycepin was found to effectively enhance activation of AMPK and inhibited activity of AKT. In all treatment groups, the expression levels of p-PI3K, p-Akt, p-p70S6K, Caspase-3, and Bcl-2 were significantly reduced, while the expression levels of p-AMPK, cleaved Caspase-3, and Bax increased, and the total levels of Akt, PI3K, and p70S6K levels remained unchanged. Overall, cordycepin was found to enhance the chemical sensitivity of esophageal cancer cells to cisplatin by inducing AMPK activation and inhibiting the AKT signaling pathway. Combination therapy of cordycepin and cisplatin represent a novel potential treatment of esophageal cancer.

Indexed as

AMP-Activated Protein KinasesAnimalsAntineoplastic AgentsCell Line, TumorCell ProliferationCisplatinDeoxyadenosinesDrug Resistance, NeoplasmEsophageal NeoplasmsProto-Oncogene Proteins c-aktAMP-Activated Protein KinasesAntineoplastic AgentsCisplatincordycepinDeoxyadenosinesProto-Oncogene Proteins c-akt

Identifiers

PMID33067427
PMCPMC7567864
OpenAlexW3093217304

What OpenQuestion holds

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Registered trials

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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.