Evidence map›Paper›PMID 29106393›Full record

ArticleOncogene2018

DHRS2 inhibits cell growth and motility in esophageal squamous cell carcinoma.

Y Zhou, L Wang, X Ban, T Zeng, Y Zhu, M Li, X-Y Guan, Y Li

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 49 citations in OpenAlex.

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  17. Turkish journal of haematology : official journal of Turkish Society of Haematology · 2020
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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 3 institutions in 2 countries.

Y ZhouState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
L WangState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
X BanState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
T ZengState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
Y ZhuState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
M LiState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
X-Y GuanState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
Y LiState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
Sun Yat-sen University Cancer Center · CNChinese University of Hong Kong · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Esophageal squamous cell carcinoma (ESCC) is highly prevailing in Asia and it is ranked in the most aggressive squamous cell carcinomas. High-frequency loss of heterozygosity occurred in chromosome 14q11.2 in many tumors including ESCC, suggesting that one or more tumor-suppressor genes might exist within this region. In this study, we identified the tumor-suppressing role of DHRS2 (short-chain dehydrogenase/reductase family, member 2) at 14q11.2 in ESCCs. Downregulation of DHRS2 occurred in 30.8% of primary ESCC tumor tissues vs paired non-tumorous tissues. DHRS2 downregulation was associated significantly with ESCC invasion, lymph nodes metastasis and clinical staging (P<0.001). Survival analysis revealed that DHRS2 downregulation was significantly associated with worse outcome of patients with ESCC. In vitro and in vivo studies indicated that both DHRS2 variants could suppress cell proliferation and cell motility. Moreover, we demonstrated that DHRS2 could reduce reactive oxygen species and decrease nicotinamide adenine dinucleotide phosphate (oxidized/reduced), increase p53 stability and decrease Rb phosphorylation; it also decreased p38 mitogen-activated protein kinase phosphorylation and matrix metalloproteinase 2. In summary, these findings demonstrated that DHRS2 had an important part in ESCC development and progression.

Indexed as

Cell MovementCell ProliferationGene Expression Regulation, NeoplasticAlcohol OxidoreductasesAnimalsApoptosisBiomarkers, TumorCarbonyl Reductase (NADPH)Carcinoma, Squamous CellCase-Control StudiesCell CycleEsophageal NeoplasmsFemaleFollow-Up StudiesHumansLymphatic MetastasisAlcohol OxidoreductasesBiomarkers, TumorCarbonyl Reductase (NADPH)DHRS2 protein, humanNuclear Proteins

Identifiers

PMID29106393
PMCPMC5851108
OpenAlexW2767273194

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.