Evidence map›Paper›PMID 40279246›Full record

ArticleCell reports2025

LncRNA SLNCR phenocopies the E2F1 DNA binding site to promote melanoma progression.

Kushani Shah, Eleni Anastasakou, Leinal Sejour, Yufei Wang, Leon Wert-Lamas, Christopher Rauchet, Sabine Studer, Simon Goller, Robert J Distel, Wayne Marasco and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Mapping rat lncRNA Bdnf-as.Molecular biology reports · 2025
    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

13 authors.

Kushani ShahDepartment of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02141, USA.
Eleni AnastasakouDepartment of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02141, USA.
Leinal SejourBroad Institute of Harvard and MIT, Cambridge, MA 02141, USA; Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.
Yufei WangDepartment of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.
Leon Wert-LamasDepartment of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02141, USA.
Christopher RauchetDepartment of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02141, USA.
Sabine StuderDepartment of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02141, USA; Department of Hematology/Oncology, Boston Children's Hospital, Boston, MA 02115, USA.
Simon GollerDepartment of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02141, USA.
Robert J DistelDepartment of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02141, USA.
Wayne MarascoDepartment of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.
Lalith PereraGenome Integrity and Structural Biology Laboratory, NIEHS, NIH, Durham, NC 27709, USA.
Ioannis S VlachosBroad Institute of Harvard and MIT, Cambridge, MA 02141, USA; Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA; Spatial Technologies Unit, Harvard Medical School Initiative for RNA Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02115, USA.
Carl D NovinaDepartment of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02141, USA. Electronic address: carl_novina@dfci.harvard.edu.

Funding

Pan-Cancer characterization of 3’UTR somatic mutations controlling tumor immune evasionR01CA258776 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI Ioannis Vlachos · 2022 to 2026
$2.9M
Defining LncRNA Function in normal and Shwachman Diamond Syndrome MyelopoiesisR01HL145714 · NHLBI · DANA-FARBER CANCER INST · PI NOVINA, CARL D · 2019 to 2022
$1.8M
Macromolecular ModelingZIAES043010 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI PEDERSEN, LEE · 2009 to 2011
$1.3M
Lnc'ing White Fat to Brown Fat ThermogenesisDP1DK126161 · NIDDK · DANA-FARBER CANCER INST · PI NOVINA, CARL D · 2020 to 2020
$885k
Intramural NIH HHS ZIA ES043010NCI NIH HHS R01 CA258776NHLBI NIH HHS R01 HL145714NIDDK NIH HHS DP1 DK126161
6 · The paper itself

Abstract

The long non-coding RNA SLNCR and the transcription factor E2F1 are known melanoma oncogenes. We show that SLNCR binds to E2F1 to promote the proliferation, invasion, and migration of melanoma cells from the bloodstream into the lungs. Blocking SLNCR-E2F1 complex formation without reducing the levels of either SLNCR or E2F1 prevents lung extravasation in mice. A 60-nt fragment of SLNCR contains two RNA analogs of the E2F1 DNA binding site (BS) in opposite orientations and can form a hairpin RNA that phenocopies the E2F1 DNA BS. Molecular dynamics (MD) simulations and biochemical experiments indicate that this fragment of SLNCR binds to the E2F1 DNA-binding domain more effectively than the E2F1 DNA BS. MD simulations predict higher affinity for DNA-E2F1 complex formation but faster kinetics and a greater number of RNA-amino acid contacts for the RNA-E2F1 complex, suggesting that RNA binding to E2F1 is more kinetically favorable.

Indexed as

Disease ProgressionDNAE2F1 Transcription FactorMelanomaRNA, Long NoncodingAnimalsBinding SitesCell Line, TumorCell MovementCell ProliferationHumansMiceMolecular Dynamics SimulationProtein BindingDNAE2F1 protein, humanE2F1 Transcription FactorRNA, Long NoncodingCP: CancerCP: GenomicsE2F1Long non-coding RNAmelanomamolecular dynamics simulationsRNA-EMSASLNCRtranscription factor-RNA binding

Identifiers

PMID40279246
PMCPMC12172627

What OpenQuestion holds

Textmetadata
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.