Evidence map›Paper›PMID 35681561›Full record

ArticleCancers2022

Targeting MUC1-C Suppresses Chronic Activation of Cytosolic Nucleotide Receptors and STING in Triple-Negative Breast Cancer.

Nami Yamashita, Atsushi Fushimi, Yoshihiro Morimoto, Atrayee Bhattacharya, Masayuki Hagiwara, Masaaki Yamamoto, Tsuyoshi Hata, Geoffrey I Shapiro, Mark D Long, Song Liu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 22 citations in OpenAlex.

  1. Wild-type C9orf72 drives proteasomal dysfunction and mutant aggregates via a Stat1-Isg15 axis in Huntington's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  2. Evolution ofInternational journal of molecular sciences · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. MUC1-C Is a Common Driver of Acquired Osimertinib Resistance in NSCLC.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2024
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. The multifaceted role of MUC1 in tumor therapy resistance.Clinical and experimental medicine · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. The Therapeutic Effects of MUC1-C shRNA@FeInternational journal of nanomedicine · 2023
    Article
  19. Review
  20. Review
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

11 authors at 2 institutions in 1 country.

Nami YamashitaDana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, D830, Boston, MA 02215, USA.
Atsushi FushimiDana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, D830, Boston, MA 02215, USA.
Yoshihiro MorimotoDana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, D830, Boston, MA 02215, USA.
Atrayee BhattacharyaDana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, D830, Boston, MA 02215, USA.
Masayuki HagiwaraDana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, D830, Boston, MA 02215, USA.
Masaaki YamamotoDana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, D830, Boston, MA 02215, USA.
Tsuyoshi HataDana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, D830, Boston, MA 02215, USA.
Geoffrey I ShapiroDana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, D830, Boston, MA 02215, USA.
Mark D LongDepartment of Biostatistics & Bioinformatics, Roswell Park Comprehensive Cancer Center,Buffalo, NY 14263, USA.ORCID 0000-0003-1120-8176
Song LiuDepartment of Biostatistics & Bioinformatics, Roswell Park Comprehensive Cancer Center,Buffalo, NY 14263, USA.
Donald KufeDana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, D830, Boston, MA 02215, USA.ORCID 0000-0001-5743-8888
Harvard University · USRoswell Park Comprehensive Cancer Center · US

Funding

Immuno-Oncology Translation Network: Data Management and Resource-Sharing Center at RPCIU24CA232979 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI HUTSON, ALAN DAVID, LIU, SONG · 2018 to 2024
$8.9M
Targeting the MUC1-C Oncoprotein in Triple-Negative Breast CancerR01CA097098 · NCI · DANA-FARBER CANCER INSTITUTE · PI DONALD W. KUFE · 2002 to 2026
$8.8M
YAP1 and RB1 cooperate to regulate lung cancer lineage plasticity and therapeutic resistanceU24CA274159 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI DAVID W. GOODRICH, Alan David Hutson · 2022 to 2026
$8.5M
MUC1-C Oncoprotein Evades Immune Destruction in Non-small Cell Lung CancerR01CA166480 · NCI · DANA-FARBER CANCER INST · PI KUFE, DONALD W., WONG, KWOK KIN · 2012 to 2021
$6.3M
MUC1-C is a Target for Reversing Immune Evasion and Resistance to ImmunotherapiesU01CA233084 · NCI · DANA-FARBER CANCER INST · PI KUFE, DONALD W., WONG, KWOK KIN · 2018 to 2022
$4.1M
NCI NIH HHS CA097098NCI NIH HHS CA166480NCI NIH HHS CA232979NCI NIH HHS CA233084NCI NIH HHS R01 CA097098NCI NIH HHS R01 CA166480NCI NIH HHS U01 CA233084NCI NIH HHS U24 CA232979NCI NIH HHS U24 CA274159
6 · The paper itself

Abstract

The MUC1-C apical transmembrane protein is activated in the acute response of epithelial cells to inflammation. However, chronic MUC1-C activation promotes cancer progression, emphasizing the importance of MUC1-C as a target for treatment. We report here that MUC1-C is necessary for intrinsic expression of the RIG-I, MDA5 and cGAS cytosolic nucleotide pattern recognition receptors (PRRs) and the cGAS-stimulator of IFN genes (STING) in triple-negative breast cancer (TNBC) cells. Consistent with inducing the PRR/STING axis, MUC1-C drives chronic IFN-β production and activation of the type I interferon (IFN) pathway. MUC1-C thereby induces the IFN-related DNA damage resistance gene signature (IRDS), which includes ISG15, in linking chronic inflammation with DNA damage resistance. Targeting MUC1-C in TNBC cells treated with carboplatin or the PARP inhibitor olaparib further demonstrated that MUC1-C is necessary for expression of PRRs, STING and ISG15 and for intrinsic DNA damage resistance. Of translational relevance, MUC1 significantly associates with upregulation of STING and ISG15 in TNBC tumors and is a target for treatment with CAR T cells, antibody-drug conjugates (ADCs) and direct inhibitors that are under preclinical and clinical development.

Indexed as

cGASISG15MUC1-CSTINGTNBC

Identifiers

PMID35681561
PMCPMC9179855
OpenAlexW4281569355

What OpenQuestion holds

Textmetadata
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.