Evidence map›Paper›PMID 31314174›Full record

ArticleMolecular oncology2019

RAC1 inhibition reverses cisplatin resistance in esophageal squamous cell carcinoma and induces downregulation of glycolytic enzymes.

Rui-Jie Zeng, Chun-Wen Zheng, Jing-E Gu, Hai-Xia Zhang, Lei Xie, Li-Yan Xu, En-Min Li

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 63 citations in OpenAlex.

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  4. Tumor-derived RAC1Science advances · 2025
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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

7 authors at 1 institution in 1 country.

Rui-Jie ZengDepartment of Biochemistry and Molecular Biology, Shantou University Medical College, China.
Chun-Wen ZhengDepartment of Biochemistry and Molecular Biology, Shantou University Medical College, China.
Jing-E GuDepartment of Biochemistry and Molecular Biology, Shantou University Medical College, China.
Hai-Xia ZhangDepartment of Biochemistry and Molecular Biology, Shantou University Medical College, China.
Lei XieDepartment of Biochemistry and Molecular Biology, Shantou University Medical College, China.
Li-Yan XuThe Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, China.
En-Min LiDepartment of Biochemistry and Molecular Biology, Shantou University Medical College, China.ORCID 0000-0001-6375-3614
Shantou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Development of chemoresistance remains a major challenge in treating esophageal squamous cell carcinoma (ESCC) patients despite treatment advances. However, the role of RAC1 in chemoresistance of ESCC and the underlying mechanisms remain largely unknown. In this study, we found that higher levels of RAC1 expression were associated with poorer prognosis in ESCC patients. Enhanced RAC1 expression increased cell proliferation, migration, and chemoresistance in vitro. Combination therapy using RAC1 inhibitor EHop-016 and cisplatin significantly promoted cell viability inhibition, G2/M phase cycle arrest, and apoptosis when compared to each monotherapy. Mechanistically, glycolysis was significantly downregulated in the RAC1 inhibitor monotherapy group and the combination group via inhibiting AKT/FOXO3a signaling when compared to the control group. Moreover, the silencing of RAC1 inhibited AKT/FOXO3a signaling and cell glycolysis while the upregulation of RAC1 produced an opposite effect. In murine xenograft models, the tumor volume and the expression of glycolytic enzymes were significantly reduced in combination therapy when compared to each monotherapy group. Overall, our study demonstrates that targeting RAC1 with an inhibitor overcomes cisplatin resistance in ESCC by suppressing glycolytic enzymes, which provides a promising strategy for treatment of ESCC in clinical practice.

Indexed as

Drug Resistance, NeoplasmEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaAnimalsCell Line, TumorCisplatinFemaleGene Expression Regulation, NeoplasticGene SilencingGlycolysisHumansMaleMiceMice, NudeMiddle AgedNeoplasm ProteinsCisplatinNeoplasm Proteinsrac1 GTP-Binding ProteinRAC1 protein, humanchemoresistancecisplatinesophageal squamous cell carcinomaglycolysisRAC1

Identifiers

PMID31314174
PMCPMC6717762
OpenAlexW2956188660

What OpenQuestion holds

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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.