Evidence map›Paper›PMID 29899406›Full record

ArticleOncogene2018

LACTB, a novel epigenetic silenced tumor suppressor, inhibits colorectal cancer progression by attenuating MDM2-mediated p53 ubiquitination and degradation.

Kaixuan Zeng, Xiaoxiang Chen, Xiuxiu Hu, Xiangxiang Liu, Tao Xu, Huiling Sun, Yuqin Pan, Bangshun He, Shukui Wang

Erratum issuedAbstract read
PubMed Publisher
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. An erratum has been issued. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
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  6. Proteostasis and Its Role in Disease Development.Cell biochemistry and biophysics · 2025
    Review
  7. Review
  8. Article
  9. The Pivotal Role of LACTB in the Process of Cancer Development.International journal of molecular sciences · 2025
    Review
  10. Review
  11. SNPs Give LACTB Oncogene-Like Functions and Prompt Tumor Progression via Dual-Regulating p53.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. CRISPR/Cas9: a powerful tool in colorectal cancer research.Journal of experimental & clinical cancer research : CR · 2023
    Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Kaixuan ZengSchool of Medicine, Southeast University, Nanjing, 210009, China.
Xiaoxiang ChenSchool of Medicine, Southeast University, Nanjing, 210009, China.
Xiuxiu HuGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, China.
Xiangxiang LiuGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, China.
Tao XuGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, China.
Huiling SunGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, China.
Yuqin PanGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, China.
Bangshun HeGeneral Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210006, China.
Shukui WangSchool of Medicine, Southeast University, Nanjing, 210009, China. sk_wang@njmu.edu.cn.ORCID http://orcid.org/0000-0001-6972-2587
Nanjing Medical University · CNSoutheast University · CNSoutheast University · BD

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is one of the most common aggressive malignancies. Like other solid tumors, inactivation of tumor suppressor genes and activation of oncogenes occur during CRC development and progression. Recently, a novel tumor suppressor, LACTB, was proposed to inhibit tumor progression, but the functional and clinical significance of this tumor suppressor in CRC remains unexplored. Herein, we found LACTB was significantly downregulated in CRC due to promoter methylation and histone deacetylation, which was associated with metastasis and advanced clinical stage. CRC patients with low LACTB expression had poorer overall survival and LACTB also determined to be an independent prognostic factor for poorer outcome. Ectopic expression of LACTB suppressed CRC cells proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro and inhibited CRC growth and metastasis in vivo, while knockout of LACTB by CRISPR/Cas9 gene editing technique resulted in an opposite phenotype. Interestingly, LACTB could exert antitumorigenic effect only in HCT116 and HCT8 cells harboring wild-type TP53, but not in HT29 and SW480 cells harboring mutant TP53 or HCT116 p53

Indexed as

Animalsbeta-LactamasesColorectal NeoplasmsDisease ProgressionEpigenesis, GeneticFemaleGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHeterograftsHumansMaleMembrane ProteinsMiceMice, Inbred BALB CMice, NudeMitochondrial Proteinsbeta-LactamasesLACTB protein, humanMDM2 protein, humanMembrane ProteinsMitochondrial ProteinsProto-Oncogene Proteins c-mdm2TP53 protein, humanTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID29899406
OpenAlexW2808355442

What OpenQuestion holds

Textmetadata
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.