Evidence map›Paper›PMID 32391354›Full record

ArticleFrontiers in cell and developmental biology2020

SOD1 Promotes Cell Proliferation and Metastasis in Non-small Cell Lung Cancer via an miR-409-3p/SOD1/SETDB1 Epigenetic Regulatory Feedforward Loop.

Shilong Liu, Bin Li, Jianyu Xu, Songliu Hu, Ning Zhan, Hong Wang, Chunzi Gao, Jian Li, Xiangying Xu

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

54 citing papers in PubMed, 73 citations in OpenAlex.

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  19. Navigating the redox landscape: reactive oxygen species in regulation of cell cycle.Redox report : communications in free radical research · 2024
    Review
  20. Bioinformatics analysis revealsTranslational cancer research · 2024
    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

9 authors at 5 institutions in 1 country.

Shilong LiuDepartment of Thoracic Radiation Oncology, The Third Affiliated Hospital of Harbin Medical University, Harbin, China.
Bin LiDepartment of Plastic Surgery, Nanfang Hospital of Southern Medical University, Guangzhou, China.
Jianyu XuDepartment of Thoracic Radiation Oncology, The Third Affiliated Hospital of Harbin Medical University, Harbin, China.
Songliu HuDepartment of Thoracic Radiation Oncology, The Third Affiliated Hospital of Harbin Medical University, Harbin, China.
Ning ZhanDepartment of Radiation Oncology, Xiang'an Hospital of Xiamen University, Xiamen, China.
Hong WangCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
Chunzi GaoDepartment of Oncology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Jian LiDepartment of Thoracic Radiation Oncology, The Third Affiliated Hospital of Harbin Medical University, Harbin, China.
Xiangying XuDepartment of Thoracic Radiation Oncology, The Third Affiliated Hospital of Harbin Medical University, Harbin, China.
Harbin Medical University · CNThird Affiliated Hospital of Harbin Medical University · CNFirst Affiliated Hospital of Harbin Medical University · CNSouthern Medical University · CNXiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Superoxide dismutase 1(SOD1) is a major antioxidant with oncogenic effects in many human cancers. Although SOD1 is overexpressed in various cancers, the clinical significance and functions of SOD1 in non-small cell lung cancer (NSCLC), particularly the epigenetic regulation of SOD1 in NSCLC carcinogenesis and progression have been less well investigated. In this study, we found that SOD1 expression was upregulated in NSCLC cell lines and tissues. Further, elevated SOD1 expression could promote NSCLC cell proliferation, invasion and migration. While inhibition of SOD1 expression induced NSCLC G1-phase cell cycle arrest and promoted apoptosis. In addition, miR-409-3p could repress SOD1 expression and significantly counteract its oncogenic activities. Bioinformatics analysis indicated that SET domain bifurcated histone lysine methyltransferase1 (SETDB1) was involved in the epigenetic regulation of miR-409-3p and SOD1 expression and functions in NSCLC cells. Identification of this miR-409-3p/SOD1/SETDB1 epigenetic regulatory feedforward loop may provide new insights into further understanding of NSCLC tumorigenesis and progression. Additionally, our results incicate that SOD1 may be a potential new therapeutic target for NSCLC treatment.

Indexed as

feedforward loopmethylationmiR-409-3pnon-small cell lung cancerSETDB1SOD1

Identifiers

PMID32391354
PMCPMC7190798
OpenAlexW3020485029

What Socratic holds

Textmetadata
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 Socratic graph.