Evidence map›Paper›PMID 16083501›Full record

ArticleMolecular cancer2005

Tumor suppressor in lung cancer 1 (TSLC1) alters tumorigenic growth properties and gene expression.

Thomas E Sussan, Mathew T Pletcher, Yoshinori Murakami, Roger H Reeves

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Non-Coding RNAs in Lung Tumor Initiation and Progression.International journal of molecular sciences · 2020
    Review
  5. Article
  6. Article
  7. Overexpression of TMEM158 contributes to ovarian carcinogenesis.Journal of experimental & clinical cancer research : CR · 2015
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Tumor suppressor TSLC1 is implicated in cell proliferation, invasion and apoptosis in laryngeal squamous cell carcinoma by regulating Akt signaling pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012
    Article
  13. Article
  14. 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

4 authors at 2 institutions in 1 country.

Thomas E SussanDepartment of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2185, USA. tsussan@jhmi.edu
Mathew T Pletcher
Yoshinori Murakami
Roger H Reeves
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

GENOMIC APPROACHES TO ANEUPLOIDYR01HD038384 · NICHD · JOHNS HOPKINS UNIVERSITY · PI REEVES, ROGER H · 2000 to 2020
$11.0M
UTILIZATION OF TRANSGENICS IN THE STUDY OF DOWN SYNDROMEP01HD024605 · NICHD · JOHNS HOPKINS UNIVERSITY · PI REEVES, ROGER H · 1989 to 2004
$8.2M
NICHD NIH HHS HD24605NICHD NIH HHS HD38384NICHD NIH HHS P01 HD024605NICHD NIH HHS R01 HD038384
6 · The paper itself

Abstract

backgroundIntroduction of cDNA or genomic clones of the tumor suppressor in lung cancer 1 (TSLC1) gene into the non-small cell lung cancer line, A549, reverses tumorigenic growth properties of these cells. These results and the observation that TSLC1 is down-regulated in a number of tumors suggest that TSLC1 functions as a critical switch mediating repression of tumorigenesis.

resultsTo investigate this mechanism, we compared growth properties of A549 with the TSLC1-containing derivative. We found a G1/S phase transition delay in 12.2. Subtractive hybridization, quantitative PCR, and TranSignal Protein/DNA arrays were used to identify genes whose expression changed when TSLC1 was up-regulated. Members of common G1/S phase regulatory pathways such as TP53, MYC, RB1 and HRAS were not differentially expressed, indicating that TSLC1 may function through an alternative pathway(s). A number of genes involved in cell proliferation and tumorigenesis were differentially expressed, notably genes in the Ras-induced senescence pathway. We examined expression of several of these key genes in human tumors and normal lung tissue, and found similar changes in expression, validating the physiological relevance of the A549 and 12.2 cell lines.

conclusionGene expression and cell cycle differences provide insights into potential downstream pathways of TSLC1 that mediate the suppression of tumor properties in A549 cells.

Indexed as

Gene Expression Regulation, NeoplasticCarcinoma, Non-Small-Cell LungCell Adhesion Molecule-1Cell Adhesion MoleculesCell DifferentiationCell Line, TumorCell ProliferationHumansImmunoglobulinsLungMembrane ProteinsProteomicsSignal TransductionTranscription FactorsTumor Suppressor ProteinsCADM1 protein, humanCell Adhesion Molecule-1Cell Adhesion MoleculesImmunoglobulinsMembrane ProteinsTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID16083501
PMCPMC1208945
OpenAlexW2126850411

What OpenQuestion holds

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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.