Evidence map›Paper›PMID 25435374›Full record

ArticleOncogene2015

SOX30, a novel epigenetic silenced tumor suppressor, promotes tumor cell apoptosis by transcriptional activating p53 in lung cancer.

F Han, W Liu, X Jiang, X Shi, L Yin, L Ao, Z Cui, Y Li, C Huang, J Cao and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

45 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. SOX on tumors, a comfort or a constraint?Cell death discovery · 2024
    Review
  10. Role of Epigenetics for the Efficacy of Cisplatin.International journal of molecular sciences · 2024
    Review
  11. Clinical Significance of SOX10 Expression in Human Pathology.Current issues in molecular biology · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

11 authors at 3 institutions in 2 countries.

F Han1] Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, PR China [2] Key Laboratory of Medical Protection for Electromagnetic Radiation, Ministry of Education of China, Chongqing, PR China.
W Liu1] Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, PR China [2] Key Laboratory of Medical Protection for Electromagnetic Radiation, Ministry of Education of China, Chongqing, PR China.
X Jiang1] Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, PR China [2] Key Laboratory of Medical Protection for Electromagnetic Radiation, Ministry of Education of China, Chongqing, PR China.
X Shi1] Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, PR China [2] Key Laboratory of Medical Protection for Electromagnetic Radiation, Ministry of Education of China, Chongqing, PR China.
L Yin1] Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, PR China [2] Key Laboratory of Medical Protection for Electromagnetic Radiation, Ministry of Education of China, Chongqing, PR China.
L Ao1] Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, PR China [2] Key Laboratory of Medical Protection for Electromagnetic Radiation, Ministry of Education of China, Chongqing, PR China.
Z Cui1] Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, PR China [2] Key Laboratory of Medical Protection for Electromagnetic Radiation, Ministry of Education of China, Chongqing, PR China.
Y Li1] Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, PR China [2] Key Laboratory of Medical Protection for Electromagnetic Radiation, Ministry of Education of China, Chongqing, PR China.
C HuangNelson Institute of Environmental Medicine, New York University School of Medicine, Tuxedo, NY, USA.
J Cao1] Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, PR China [2] Key Laboratory of Medical Protection for Electromagnetic Radiation, Ministry of Education of China, Chongqing, PR China.
J Liu1] Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing, PR China [2] Key Laboratory of Medical Protection for Electromagnetic Radiation, Ministry of Education of China, Chongqing, PR China.
Army Medical University · CNMinistry of Education of the People's Republic of China · CNNew York University · US

Funding

Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ADRIANA HEGUY · 1985 to 2026
$83.1M
NCI NIH HHS P30 CA016087
6 · The paper itself

Abstract

Although members of SOX family have been well documented for their essential roles in embryonic development, cell proliferation and disease, the functional role and molecular mechanism of SOX30 in cancer are largely unexplored. Here, we first identified SRY-box containing gene 30 (SOX30) as a novel preferentially methylated gene using genome-wide methylation screening. SOX30 hypermethylation was detected in 100% of lung cancer cell lines (9/9) and 70.83% (85/120) of primary lung tumor tissues compared with none (0/20) of normal and 8.0% (2/25) of peri-tumoral lung tissues (P<0.01). SOX30 was expressed in normal and peri-tumoral lung tissues in which SOX30 was unmethylated, but was silenced or downregulated in lung cancer cell lines and primary lung tumor tissues harboring a hypermethylated SOX30. De-methylation experiments further confirmed that silence of SOX30 was regulated by its hypermethylation. Ectopic expression of SOX30 induces cancer cell apoptosis with inhibiting proliferation in vitro and represses tumor formation in vivo, whereas knockdown of SOX30 demonstrates a reversed effect both in vitro and in vivo. At the molecular level, the antitumorigenic effect of SOX30 is mediated by directly binding to CACTTTG (+115 to +121) of p53 promoter region and activating p53 transcription, suggesting that SOX30 is a novel transcriptional activating factor of p53. Indeed, blockade of p53 attenuates the tumor inhibition of SOX30. Overall, these findings demonstrate that SOX30 is a novel epigenetic silenced tumor suppressor acting through direct regulation of p53 transcription and expression. This study provides novel insights on the mechanism of tumorigenesis in lung cancer.

Indexed as

ApoptosisCarcinogenesisCell Line, TumorCell MovementCell ProliferationDNA MethylationDown-RegulationEpigenesis, GeneticEpigenomicsGene Expression Regulation, NeoplasticGene SilencingGenes, Tumor SuppressorHumansLung NeoplasmsPromoter Regions, GeneticSOX Transcription FactorsSOX Transcription FactorsTumor Suppressor Protein p53

Identifiers

PMID25435374
PMCPMC4541146
OpenAlexW1971043408

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.