Evidence map›Paper›PMID 22505454›Full record

ArticleThe Journal of clinical investigation2012

ERK3 signals through SRC-3 coactivator to promote human lung cancer cell invasion.

Weiwen Long, Charles E Foulds, Jun Qin, Jian Liu, Chen Ding, David M Lonard, Luisa M Solis, Ignacio I Wistuba, Jun Qin, Sophia Y Tsai and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

84 citing papers in PubMed, 168 citations in OpenAlex.

  1. Trial
  2. Intracellular pH regulates ubiquitin-mediated degradation of the MAP kinase ERK3.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Atypical MAPKs in cancer.The FEBS journal · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
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  14. Review
  15. Review
  16. Steroid receptor coactivator 3 is a key modulator of regulatory T cell-mediated tumor evasion.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  17. Article
  18. ERK3 and DGKζ interact to modulate cell motility in lung cancer cells.Frontiers in cell and developmental biology · 2023
    Article
  19. Article
  20. Signaling pathways and therapeutic interventions in gastric cancer.Signal transduction and targeted therapy · 2022
    Review

24 more citing papers are in PubMed but not listed here.

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

12 authors at 2 institutions in 2 countries.

Weiwen LongDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA.
Charles E Foulds
Jun Qin
Jian Liu
Chen Ding
David M Lonard
Luisa M Solis
Ignacio I Wistuba
Jun Qin
Sophia Y Tsai
Ming-Jer Tsai
Bert W O'Malley
Baylor College of Medicine · USThe University of Texas MD Anderson Cancer Center · US

Funding

ProteomicsU19DK062434 · NIDDK · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI O'MALLEY, BERT W · 2002 to 2011
$37.4M
UNDERSTANDING FXTAS AMONG MALES WITH THE FMR1 PREMUTATIONP30HD024064 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI BEAUDET, ARTHUR L. · 1988 to 2013
$29.4M
REPRODUCTIVE HORMONES: BIOLOGICAL AND MOLECULAR ACTIONSR01HD008188 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI DAVID M LONARD, JOHN P LYDON · 1985 to 2026
$16.3M
SEX HORMONE RECEPTOR COMPONENTS AND THE CELL GENOMER01HD007857 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI DAVID M LONARD, JOHN P LYDON · 1985 to 2026
$14.6M
Diabetes Endocrinology Research CenterP30DK079638 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI CHAN, LAWRENCE · 2008 to 2012
$6.4M
SEX HORMONE RECEPTOR COMPONENTS &THE CELL GENOMER37HD007857 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI MC KEOWN, MICHAEL B · 1987 to 1996
–
NICHD NIH HHS 5R01HD-8188NICHD NIH HHS HD07857NICHD NIH HHS R01 HD007857NICHD NIH HHS R01 HD008188NIDDK NIH HHS 2U19DK062434NIDDK NIH HHS P30 DK079638NIDDK NIH HHS U19 DK062434
6 · The paper itself

Abstract

In contrast to the well-studied classic MAPKs, such as ERK1/2, little is known concerning the regulation and substrates of the atypical MAPK ERK3 signaling cascade and its function in cancer progression. Here, we report that ERK3 interacted with and phosphorylated steroid receptor coactivator 3 (SRC-3), an oncogenic protein overexpressed in multiple human cancers at serine 857 (S857). This ERK3-mediated phosphorylation at S857 was essential for interaction of SRC-3 with the ETS transcription factor PEA3, which promotes upregulation of MMP gene expression and proinvasive activity in lung cancer cells. Importantly, knockdown of ERK3 or SRC-3 inhibited the ability of lung cancer cells to invade and form tumors in the lung in a xenograft mouse model. In addition, ERK3 was found to be highly upregulated in human lung carcinomas. Our study identifies a previously unknown role for ERK3 in promoting lung cancer cell invasiveness by phosphorylating SRC-3 and regulating SRC-3 proinvasive activity by site-specific phosphorylation. As such, ERK3 protein kinase may be an attractive target for therapeutic treatment of invasive lung cancer.

Indexed as

AnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementFemaleGene Expression Regulation, NeoplasticHumansLung NeoplasmsMAP Kinase Signaling SystemMatrix MetalloproteinasesMiceMice, SCIDMitogen-Activated Protein Kinase 6Neoplasm InvasivenessNeoplasm TransplantationNuclear Receptor Coactivator 3Matrix MetalloproteinasesMitogen-Activated Protein Kinase 6NCOA3 protein, humanNuclear Receptor Coactivator 3transcription factor PEA3Transcription Factors

Identifiers

PMID22505454
PMCPMC3336992
OpenAlexW2103574630

What OpenQuestion holds

Textmetadata
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.