Evidence map›Paper›PMID 38740827›Full record

ArticleCell death & disease2024

XIST and MUC1-C form an auto-regulatory pathway in driving cancer progression.

Keyi Wang, Atrayee Bhattacharya, Naoki Haratake, Tatsuaki Daimon, Ayako Nakashoji, Hiroki Ozawa, Bo Peng, Wei Li, Donald Kufe

Abstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. The Emerging Role of METTL3 in Lung Diseases.International journal of molecular sciences · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Bioinformatics-based prognostic value andFrontiers in oncology · 2025
    Article
  10. 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

9 authors.

Keyi Wang *Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.ORCID 0000-0001-5656-2115
Atrayee Bhattacharya *Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Naoki HaratakeDana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Tatsuaki DaimonDana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Ayako NakashojiDana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Hiroki OzawaDana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-3771-7940
Bo PengDepartment of Urology, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China.
Wei LiDepartment of Urology, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China. weili06@tongi.edu.cn.
Donald KufeDana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA. donald_kufe@dfci.harvard.edu.ORCID 0000-0001-5743-8888

Funding

Targeting the MUC1-C Oncoprotein in Triple-Negative Breast CancerR01CA097098 · NCI · DANA-FARBER CANCER INSTITUTE · PI DONALD W. KUFE · 2002 to 2026
$8.8M
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
Targeting MUC1-C with an antibody drug conjugate for the therapy of advanced prostate cancerR21CA262991 · NCI · DANA-FARBER CANCER INST · PI KUFE, DONALD W. · 2022 to 2022
$442k
Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.) CA233084Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.) CA262991Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.) CA97098NCI NIH HHS R01 CA097098NCI NIH HHS R21 CA262991NCI NIH HHS U01 CA233084
6 · The paper itself

Abstract

The long non-coding RNA X-inactive specific transcript (lncRNA XIST) and MUC1 gene are dysregulated in chronic inflammation and cancer; however, there is no known interaction of their functions. The present studies demonstrate that MUC1-C regulates XIST lncRNA levels by suppressing the RBM15/B, WTAP and METTL3/14 components of the m6A methylation complex that associate with XIST A repeats. MUC1-C also suppresses the YTHDF2-CNOT1 deadenylase complex that recognizes m6A sites and contributes to XIST decay with increases in XIST stability and expression. In support of an auto-regulatory pathway, we show that XIST regulates MUC1-C expression by promoting NF-κB-mediated activation of the MUC1 gene. Of significance, MUC1-C and XIST regulate common genes associated with inflammation and stemness, including (i) miR-21 which is upregulated across pan-cancers, and (ii) TDP-43 which associates with the XIST E repeats. Our results further demonstrate that the MUC1-C/XIST pathway (i) is regulated by TDP-43, (ii) drives stemness-associated genes, and (iii) is necessary for self-renewal capacity. These findings indicate that the MUC1-C/XIST auto-regulatory axis is of importance in cancer progression.

Indexed as

Gene Expression Regulation, NeoplasticMucin-1RNA, Long NoncodingAnimalsCell Line, TumorDisease ProgressionDNA-Binding ProteinsHumansMiceMicroRNAsNeoplasmsNF-kappa BDNA-Binding ProteinsMicroRNAsMUC1 protein, humanMucin-1NF-kappa BRNA, Long NoncodingXIST non-coding RNA

Identifiers

PMID38740827
PMCPMC11091074

What OpenQuestion holds

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Registered trials

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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.