Evidence map›Paper›PMID 22890320›Full record

ArticleOncogene2013

Sin3a acts through a multi-gene module to regulate invasion in Drosophila and human tumors.

T K Das, J Sangodkar, N Negre, G Narla, R L Cagan

Abstract read
In one paragraph

Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
2.1field-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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Silencing of the long non-coding RNAOncology research · 2024
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  9. Review
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  18. Review
  19. Large-Scale TransgenicGenetics · 2020
    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

5 authors at 2 institutions in 1 country.

T K DasDepartment of Developmental and Regenerative Biology, Mount Sinai School of Medicine, New York, NY, USA.
J Sangodkar
N Negre
G Narla
R L Cagan
Icahn School of Medicine at Mount Sinai · USUniversity of Chicago · US

Funding

T32 training grant in medical genetics.T32GM082773 · NIGMS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Laszlo Tamas Kozicz, Eva Morava-Kozicz · 2008 to 2026
$4.9M
A Drosophila Model for Src-Mediated OncogenesisR01CA109730 · NCI · WASHINGTON UNIVERSITY · PI CAGAN, ROSS LEIGH · 2004 to 2013
$2.9M
A DROSOPHILA MODEL FOR MEN2B AND SPORADIC MTCR01CA084309 · NCI · WASHINGTON UNIVERSITY · PI CAGAN, ROSS LEIGH · 2000 to 2009
$2.0M
A Drosophila Model Linking Diet-induced Obesity and Cancer (PQ 1)R01CA170495 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CAGAN, ROSS LEIGH · 2012 to 2015
$1.4M
NCI NIH HHS R01 CA084309NCI NIH HHS R01-CA084309NCI NIH HHS R01 CA109730NCI NIH HHS R01-CA109730NCI NIH HHS R01 CA170495NIGMS NIH HHS T32 GM082773
6 · The paper itself

Abstract

Chromatin remodeling proteins regulate multiple aspects of cell homeostasis, making them ideal candidates for misregulation in transformed cells. Here, we explore Sin3A, a member of the Sin3 family of proteins linked to tumorigenesis that are thought to regulate gene expression through their role as histone deacetylases (HDACs). We identified Drosophila Sin3a as an important mediator of oncogenic Ret receptor in a fly model of Multiple Endocrine Neoplasia Type 2. Reducing Drosophila Sin3a activity led to metastasis-like behavior and, in the presence of Diap1, secondary tumors distant from the site of origin. Genetic and Chip-Seq analyses identified previously undescribed Sin3a targets including genes involved in cell motility and actin dynamics, as well as signaling pathways including Src, Jnk and Rho. A key Sin3a oncogenic target, PP1B, regulates stability of β-Catenin/Armadillo: the outcome is to oppose T-cell factor (TCF) function and Wg/Wnt pathway signaling in both fly and mammalian cancer cells. Reducing Sin3A strongly increased the invasive behavior of A549 human lung adenocarcinoma cells. We show that Sin3A is downregulated in a variety of human tumors and that Src, JNK, RhoA and PP1B/β-Catenin are regulated in a manner analogous to our Drosophila models. Our data suggest that Sin3A influences a specific step of tumorigenesis by regulating a module of genes involved in cell invasion. Tumor progression may commonly rely on such 'modules of invasion' under the control of broad transcriptional regulators.

Indexed as

Animalsbeta CateninCell Line, TumorCell MovementCell Transformation, NeoplasticDrosophilaDrosophila ProteinsGene Expression Regulation, NeoplasticHumansInhibitor of Apoptosis ProteinsJNK Mitogen-Activated Protein KinasesLung NeoplasmsMultiple Endocrine Neoplasia Type 2aNeoplasm InvasivenessProto-Oncogene Proteins c-retRepressor Proteinsbeta CateninDIAP1 protein, DrosophilaDrosophila ProteinsInhibitor of Apoptosis ProteinsJNK Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-retRepressor ProteinsRet protein, DrosophilarhoA GTP-Binding ProteinSIN3A transcription factorSin3 Histone Deacetylase and Corepressor Complexsrc-Family Kinaseswg protein, DrosophilaWnt1 Protein

Identifiers

PMID22890320
PMCPMC3696049
OpenAlexW1985092406

What OpenQuestion holds

Textmetadata
LicenceTDM
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.