Evidence map›Paper›PMID 32896989›Full record

ArticleJournal of cellular and molecular medicine2020

LMNA functions as an oncogene in hepatocellular carcinoma by regulating the proliferation and migration ability.

Heng Liu, Dongming Li, Ling Zhou, Shuang Kan, Guozhang He, Kun Zhou, Liping Wang, Ming Chen, Wei Shu

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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

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  11. Knockdown ofCell adhesion & migration · 2023
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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

9 authors at 4 institutions in 1 country.

Heng LiuCollege of Biotechnology, Guilin Medical University, Guilin, China.
Dongming LiDepartment of Cell Biology and Genetics, Guangxi Medical University, Nanning, China.
Ling ZhouDepartment of Cell Biology and Genetics, Guangxi Medical University, Nanning, China.
Shuang KanState Key Laboratory for the Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmacy, Guangxi Normal University, Guilin, China.
Guozhang HeState Key Laboratory for the Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmacy, Guangxi Normal University, Guilin, China.
Kun ZhouDepartment of General Surgery, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Liping WangCollege of Biotechnology, Guilin Medical University, Guilin, China.ORCID 0000-0001-6372-5939
Ming ChenState Key Laboratory for the Chemistry and Molecular Engineering of Medicinal Resources, School of Chemistry and Pharmacy, Guangxi Normal University, Guilin, China.ORCID 0000-0001-5935-7694
Wei ShuCollege of Biotechnology, Guilin Medical University, Guilin, China.
Guangxi Medical University · CNGuangxi Normal University · CNGuilin Medical University · CNThird Affiliated Hospital of Southern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of the LMNA gene in the development and progression of hepatocellular carcinoma (HCC) and the associated molecular mechanism is not yet clear. Therefore, the purpose of this study was to evaluate the relationship between LMNA and HCC. LMNA gene expression in normal tissues and corresponding tumours was evaluated and the Kaplan-Meier survival analysis was performed. Next, the LMNA gene was knocked out in the 293T and HepG2 cell lines using the CRISPR/Cas9 technique. Subsequently, the proliferation, migration and colony formation rate of the two LMNA knockout cell lines were analysed. Finally, the molecular mechanism affecting the tumorigenesis due to the loss of the LMNA gene was evaluated. The results showed that the LMNA gene was abnormally expressed in many tumours, and the survival rate of the HCC patients with a high expression of the LMNA gene was significantly reduced compared with the rate in patients with a low LMNA expression. The knockout of the LMNA gene in the HCC cell line HepG2 resulted in a decreased tumorigenicity, up-regulation of the P16 expression and down-regulation of the CDK1 expression. These findings suggested that LMNA might function as an oncogene in HCC and provided a potential new target for the diagnosis and treatment of HCC.

Indexed as

Cell MovementOncogenesAnimalsApoptosisBase SequenceCarcinoma, HepatocellularCell Cycle CheckpointsCell ProliferationCRISPR-Cas SystemsExtracellular MatrixGene Expression Regulation, NeoplasticHEK293 CellsHep G2 CellsHumansLamin Type ALiver NeoplasmsLamin Type ACRISPR/Cas9Hepatocellular carcinoma (HCC)LMNAP16

Identifiers

PMID32896989
PMCPMC7578910
OpenAlexW3084297414

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.