Evidence map›Paper›PMID 33473104›Full record

ArticleSignal transduction and targeted therapy2021

Targeting Notch and EGFR signaling in human mucoepidermoid carcinoma.

Wei Ni, Zirong Chen, Xin Zhou, Rongqiang Yang, Mu Yu, Jianrong Lu, Frederic J Kaye, Lizi Wu

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Potassium Iodide Induces Apoptosis in Salivary Gland Cancer Cells.International journal of molecular sciences · 2025
    Article
  3. Review
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  14. Targeted therapy for rare lung cancers: Status, challenges, and prospects.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Review
  15. Article
  16. Article
  17. The Therapeutic Landscape of Salivary Gland Malignancies-Where Are We Now?International journal of molecular sciences · 2022
    Review
  18. Article
  19. Diagnostic Value of MAML2 Rearrangements in Mucoepidermoid Carcinoma.International journal of molecular sciences · 2022
    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

8 authors at 1 institution in 1 country.

Wei NiDepartment of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL, 32610, USA.ORCID 0000-0002-5729-827X
Zirong ChenDepartment of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL, 32610, USA.
Xin ZhouDepartment of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL, 32610, USA.
Rongqiang YangDepartment of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL, 32610, USA.
Mu YuDepartment of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL, 32610, USA.
Jianrong LuUF Health Cancer Center, University of Florida, Gainesville, FL, 32610, USA.
Frederic J KayeUF Health Cancer Center, University of Florida, Gainesville, FL, 32610, USA.
Lizi WuDepartment of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL, 32610, USA. lzwu@ufl.edu.ORCID 0000-0002-0076-2617
University of Florida Health · US

Funding

Signaling and Targeting of CRTC1-MAML2 Fusion Oncoprotein in Salivary Gland TumorR01DE023641 · NIDCR · UNIVERSITY OF FLORIDA · PI Lizi Wu · 2014 to 2026
$3.3M
Aberrant CRTC activation as a unique vulnerability of lung cancer with LKB1 inactivationR01CA234351 · NCI · UNIVERSITY OF FLORIDA · PI WU, LIZI · 2019 to 2023
$1.7M
NCI NIH HHS R01 CA234351NIDCR NIH HHS R01 DE023641
6 · The paper itself

Abstract

Mucoepidermoid carcinoma (MEC) is the most common type of salivary gland cancers and patients with advanced, metastatic, and recurrent MECs have limited therapeutic options and poor treatment outcomes. MEC is commonly associated with a chromosomal translocation t(11;19) (q14-21;p12-13) that encodes the CRTC1-MAML2 oncogenic fusion. The CRTC1-MAML2 fusion is required for MEC growth in part through inducing autocrine AREG-EGFR signaling. Growing evidence suggests that MEC malignancy is maintained by cancer stem-like cells. In this study, we aimed to determine critical signaling for maintaining MEC stem-like cells and the effect of combined targeting of stem cell signaling and CRTC1-MAML2-induced EGFR signaling on blocking MEC growth. First, we evaluated the significance of Notch signaling in regulating MEC stem-like cells. Aberrantly activated Notch signaling was detected in human fusion-positive MEC cells. The inhibition of Notch signaling with genetic or pharmacological inhibitors reduced oncosphere formation and ALDH-bright population in vitro and blocked the growth of MEC xenografts in vivo. Next, we investigated the effect of co-targeting Notch signaling and EGFR signaling, and observed enhanced inhibition on MEC growth in vivo. Collectively, this study identified a critical role of Notch signaling in maintaining MEC stem-like cells and tumor growth, and revealed a novel approach of co-targeting Notch and EGFR signaling as a potential effective anti-MEC treatment.

Indexed as

AnimalsCarcinoma, MucoepidermoidCell ProliferationErbB ReceptorsErlotinib HydrochlorideHeterograftsHumansMiceMolecular Targeted TherapyNeoplastic Stem CellsOncogene Proteins, FusionReceptors, NotchSalivary Gland NeoplasmsSignal TransductionTrans-ActivatorsTranscription FactorsCRTC1 protein, humanEGFR protein, humanErbB ReceptorsErlotinib HydrochlorideMAML2 protein, humanOncogene Proteins, FusionReceptors, NotchTrans-ActivatorsTranscription Factors

Identifiers

PMID33473104
PMCPMC7817832
OpenAlexW3125713104

What OpenQuestion holds

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LicenceCC BY
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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.