Evidence map›Paper›PMID 35925486›Full record

ArticleMolecular biology reports2022

α-Enolase inhibits apoptosis and promotes cell invasion and proliferation of skin cutaneous melanoma.

Kun Zhang, Ruoxi Tian, Wancong Zhang, Yishuai Li, Ning Zeng, Yan Liang, Shijie Tang

Open access · hybridAbstract read
In one paragraph

Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. mFrontiers in cell and developmental biology · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Role of ENO1 and its targeted therapy in tumors.Journal of translational medicine · 2024
    Review
  9. Review
  10. Article
  11. Article
  12. 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

7 authors at 5 institutions in 1 country.

Kun Zhang *Department of Plastic Surgery and Burn Center, Second Affiliated Hospital, Shantou University Medical College, Shantou, Guangdong, China.
Ruoxi Tian *School of Basic Medicine, Tianjin Medical University, Tianjin, China.
Wancong ZhangDepartment of Plastic Surgery and Burn Center, Second Affiliated Hospital, Shantou University Medical College, Shantou, Guangdong, China.
Yishuai LiDepartment of Thoracic Surgery, Hebei Chest Hospital, Shijiazhuang, Hebei, China.
Ning ZengDepartment of Nephrology, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Yan LiangDepartment of Plastic Surgery and Burn Center, Second Affiliated Hospital, Shantou University Medical College, Shantou, Guangdong, China. yan.liang524@hotmail.com.
Shijie TangDepartment of Plastic Surgery and Burn Center, Second Affiliated Hospital, Shantou University Medical College, Shantou, Guangdong, China. sjtang3@stu.edu.cn.
Second Affiliated Hospital of Shantou University Medical College · CNGuilin Medical University · CNHospital of Hebei Province · CNShantou University · CNTianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe glycolytic enzyme, α-Enolase (ENO1), catalyzes the production of phosphoenolpyruvate from 2-phosphoglycerate, thereby enhancing glycolysis and contributing to tumor progression. In the present study, we aimed to determine the role of ENO1 in skin cutaneous melanoma (SKCM) and the potential underlying mechanism.

methodsThe Sangerbox database was used to analyze the mRNA expression of ENO1 in SKCM. Western blotting was used to assess the levels of ENO1, c-Myc, β-catenin, MMP-9, PGAM1, and MMP-13 in SKCM-derived cell lines or tumor tissues from patients with SKCM. The pCMV-SPORT6-ENO1 and pET-28a-ENO1siRNA plasmids were used to overexpress and knockdown ENO1 in SKCM cells, respectively. To determine the function of ENO1 in the malignant behavior of SKCM cells, we performed a wound-healing assay, cell counting kit 8 assay, and transwell chamber analyses. The production of pyruvate and lactic acid in tumor cells was evaluated using their respective kits.

resultsCompared with non-tumor tissues, ENO1 was found to be overexpressed in SKCM tissues. In SKCM cells, ENO1 overexpression promoted invasion, migration, and proliferation of tumor cells; increased pyruvate and lactate production; and increased β-catenin, MMP-9, MMP-13, and c-Myc levels. The opposite effects were observed in SKCM cells silenced for ENO1.

conclusionsThese results indicate that ENO1 is involved in SKCM progression by enhancing the invasion and proliferation of tumor cells. In addition, ENO1 might have an important function in tumor cell glycolysis. Therefore, ENO1 represents a potential therapeutic target for treatment of SKCM.

Indexed as

MelanomaSkin NeoplasmsApoptosisbeta CateninBiomarkers, TumorCell Line, TumorCell ProliferationCutaneous Malignant MelanomaHumansMatrix Metalloproteinase 13Matrix Metalloproteinase 9Phosphopyruvate HydratasePyruvatesbeta CateninBiomarkers, TumorMatrix Metalloproteinase 13Matrix Metalloproteinase 9Phosphopyruvate HydratasePyruvatesENO1InvasionMigrationProliferationSKCM

Identifiers

PMID35925486
PMCPMC9463226
OpenAlexW4289779390

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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.