Evidence map›Paper›PMID 32678482›Full record

ArticleJournal of cellular and molecular medicine2020

AKR1C2 acts as a targetable oncogene in esophageal squamous cell carcinoma via activating PI3K/AKT signaling pathway.

Zhan-Fei Zhang, Tie-Jun Huang, Xin-Ke Zhang, Yu-Jie Xie, Si-Ting Lin, Fei-Fei Luo, Dong-Fang Meng, Hao Hu, Jing Wang, Li-Xia Peng and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

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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

13 authors at 3 institutions in 1 country.

Zhan-Fei ZhangDepartment of Thoracic Surgery, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Tie-Jun HuangDepartment of Experimental Research, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Xin-Ke ZhangDepartment of Nuclear Medicine, The Second People's Hospital of Shenzhen, Shenzhen, China.
Yu-Jie XieDepartment of Nasopharyngeal Carcinoma, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Si-Ting LinDepartment of Pathology, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Fei-Fei LuoDepartment of Pathology, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Dong-Fang MengDepartment of Pathology, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Hao HuDepartment of Thoracic Surgery, The People's Hospital of Gaozhou, Maoming, China.
Jing WangDepartment of Pathology, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Li-Xia PengDepartment of Pathology, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Chao-Nan QianDepartment of Experimental Research, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China.
Chao ChengDepartment of Thoracic Surgery, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Bi-Jun HuangDepartment of Pathology, Sun Yat-Sen University Cancer Center, Guangzhou, China.ORCID 0000-0001-6816-1503
Sun Yat-sen University · CNGaozhou People's Hospital · CNShenzhen Second People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aldo-keto reductases family 1 member C2 (AKR1C2) has critical roles in the tumorigenesis and progression of malignant tumours. However, it was also discovered to have ambiguous functions in multiple cancers and till present, its clinical significance and molecular mechanism in oesophageal squamous cell carcinoma (ESCC) has been unclear. The aim of this study was to explore the role of AKR1C2 in the tumorigenesis of ESCC. Here, we showed that AKR1C2 expression was found to be up-regulated in ESCC tissues and was significantly associated with pathological stage, lymph node metastasis and worse outcomes. Functional assays demonstrated that an ectopic expression of AKR1C2 in ESCC cells resulted in increased proliferation, migration and cisplatin resistance, while knockdown led to inversing effects. Bioinformation analyses and mechanistic studies demonstrated that AKR1C2 activated the PI3K/AKT signalling pathway, furthermore, the inhibitor of PI3K or the selective inhibitor of AKR1C2 enzyme activity could reverse the aggressiveness and showed synergistic antitumour effect when combined with cisplatin, both in vitro and in vivo. In conclusion, Our findings revealed that AKR1C2 could function as an oncogene by activating the PI3K/AKT pathway, as a novel prognostic biomarker and/or as a potential therapeutic target to ESCC.

Indexed as

3-alpha-Hydroxysteroid Dehydrogenase (B-Specific)AnimalsAntineoplastic AgentsBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationCisplatinDrug Resistance, NeoplasmEsophageal Squamous Cell CarcinomaFemaleGene Expression Regulation, NeoplasticHumansHydroxysteroid DehydrogenasesLymphatic MetastasisMale3-alpha-Hydroxysteroid Dehydrogenase (B-Specific)AKR1C2 protein, humanAntineoplastic AgentsBiomarkers, TumorCisplatinHydroxysteroid DehydrogenasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAKR1C2cisplatin resistancecombination therapyoesophageal squamous cell carcinomaPI3K/AKT signalling pathway

Identifiers

PMID32678482
PMCPMC7520259
OpenAlexW3043651941

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.