Evidence map›Paper›PMID 35712471›Full record

ArticleFrontiers in oncology2022

Knockdown of LMNB1 Inhibits the Proliferation of Lung Adenocarcinoma Cells by Inducing DNA Damage and Cell Senescence.

Jiangbo Li, Zhijia Sun, Yingshu Cui, Lingmei Qin, Fengyun Wu, Yufang Li, Nan Du, Xiaosong Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Postbiotic metabolites fromExperimental and therapeutic medicine · 2026
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  5. Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026
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  9. International journal of molecular sciences · 2025
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. LMNB1 targets FOXD1 to promote progression of prostate cancer.Experimental and therapeutic medicine · 2023
    Article
  16. Article
  17. Article
  18. 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

8 authors at 3 institutions in 1 country.

Jiangbo LiDepartment of Biology, Beijing Institute of Biotechnology, Beijing, China.
Zhijia SunMedical School of Chinese People's Liberation Army (PLA), Chinese People's Liberation Army General Hospital, Beijing, China.
Yingshu CuiMedical School of Chinese People's Liberation Army (PLA), Chinese People's Liberation Army General Hospital, Beijing, China.
Lingmei QinDepartment of Biology, Beijing Institute of Biotechnology, Beijing, China.
Fengyun WuCollege of Life Sciences, Capital Normal University, Beijing, China.
Yufang LiCollege of Life Sciences, Capital Normal University, Beijing, China.
Nan DuDepartment of Oncology, Fourth Medical Center of Chinese PLA General Hospital, Chinese People's Liberation Army General Hospital, Beijing, China.
Xiaosong LiDepartment of Oncology, Fourth Medical Center of Chinese PLA General Hospital, Chinese People's Liberation Army General Hospital, Beijing, China.
Capital Normal University · CNChinese People's Liberation Army · CNChinese PLA General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Lung cancer has considerably high mortality and morbidity rate. Lung adenocarcinoma (LUAD) tissues highly express lamin B1 (LMNB1), compared with normal tissues. In this study, we knocked down LMNB1 in LUAD cells A549 and NCI-1299 to explore the effect of its inhibition on the proliferation of cells and the potential mechanism. Methods: Using bioinformatics methods, we analyzed the specificity of LMNB1 mRNA expression level in LUAD and its effect on prognosis from TCGA data. SiRNAs were used to knock down LMNB1 in the A549 cell line, and the knockdown effect was identified by western blotting and qRT-PCR. Through CCK8 cell proliferation assay, wound healing assay, TRAP, cloning formation Assay, DNase I-TUNEL assay, ATAC-seq, immunofluorescence, FISH, Results: According to bioinformatics analysis, LMNB1 is substantially abundant in LUAD tissues and is associated with tumor stage and patient survival (P < 0.05). After silencing LMNB1, the rate of cell growth, wound healing, the number of transwells, and the number of cell colonies all decreased significantly (P < 0.01). With the decreased LMNB1 expression, H3K9me3 protein expression decreases, chromosome accessibility increases, P53, P21, P16 and γ-H2AX protein expression increases, and the number of senescence staining positive cells increases. At the same time, Conclusions: Overexpression of LMNB1 in LUAD cells is significant, which has excellent potential to be an indicator for evaluating the clinical prognosis of LUAD patients and a target for precise treatment.

Indexed as

cell senescencechromosome accessibilityLMNB1LUADtelomere

Identifiers

PMID35712471
PMCPMC9194513
OpenAlexW4285744710

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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.