Evidence map›Paper›PMID 23552700›Full record

ArticleOncogenesis2012

The tumor suppressor RASSF10 is upregulated upon contact inhibition and frequently epigenetically silenced in cancer.

A M Richter, S K Walesch, P Würl, H Taubert, R H Dammann

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

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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 3 institutions in 1 country.

A M RichterInstitute for Genetics, Justus-Liebig-University, Universities of Giessen and Marburg Lung Center, Member of the German Center for Lung Research, Giessen, Germany.
S K Walesch
P Würl
H Taubert
R H Dammann
German Center for Lung Research · DEEvangelisches Diakoniekrankenhaus · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Ras association domain family (RASSF) comprises a group of tumor suppressors that are frequently epigenetically inactivated in various tumor entities and linked to apoptosis, cell cycle control and microtubule stability. In this work, we concentrated on the newly identified putative tumor suppressor RASSF10. Methylation analysis reveals RASSF10 promoter hypermethylation in lung cancer, head and neck (HN) cancer, sarcoma and pancreatic cancer. An increase in RASSF10 methylation from normal tissues, primary tumors to cancer cell lines was observed. Methylation was reversed by 5-aza-2'-deoxycytidine treatment leading to reexpression of RASSF10. We further show that overexpression of RASSF10 suppresses colony formation in cancer cell lines. In addition, RASSF10 is upregulated by cell-cell contact and regulated on promoter level as well as endogenously by forskolin, protein kinase A (PKA) and activator Protein 1 (AP-1), linking RASSF10 to the cAMP signaling pathway. Knockdown of the AP-1 member JunD interfered with contact inhibition induced RASSF10 expression. In summary, we found RASSF10 to be epigenetically inactivated by hypermethylation of its CpG island promoter in lung, HN, sarcoma and pancreatic cancer. Furthermore, our novel findings suggest that tumor suppressor RASSF10 is upregulated by PKA and JunD signaling upon contact inhibition and that RASSF10 suppresses growth of cancer cells.

Identifiers

PMID23552700
PMCPMC3412644
OpenAlexW1999442619

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.