Evidence map›Paper›PMID 39259576›Full record

ArticleeLife2024

Targeting ribosome biogenesis as a novel therapeutic approach to overcome EMT-related chemoresistance in breast cancer.

Yi Ban, Yue Zou, Yingzhuo Liu, Sharrel Lee, Robert B Bednarczyk, Jianting Sheng, Yuliang Cao, Stephen T C Wong, Dingcheng Gao

Abstract read
In one paragraph

Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
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  5. EMT and cancer stem cells: Drivers of therapy resistance and promising therapeutic targets.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2025
    Review
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  14. Spatially Informed Graph Structure Learning Extracts Insights from Spatial Transcriptomics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  15. Article
  16. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Yi Ban *Department of Cardiothoracic Surgery, Weill Cornell Medicine, New York, United States.ORCID https://orcid.org/0000-0002-7644-9686
Yue Zou *Department of Cardiothoracic Surgery, Weill Cornell Medicine, New York, United States.
Yingzhuo LiuDepartment of Cardiothoracic Surgery, Weill Cornell Medicine, New York, United States.
Sharrel LeeDepartment of Cardiothoracic Surgery, Weill Cornell Medicine, New York, United States.
Robert B BednarczykDepartment of Cardiothoracic Surgery, Weill Cornell Medicine, New York, United States.
Jianting ShengSystems Medicine and Bioengineering Department, Houston Methodist Cancer Center, Houston Methodist Hospital, Houston, United States.
Yuliang CaoSystems Medicine and Bioengineering Department, Houston Methodist Cancer Center, Houston Methodist Hospital, Houston, United States.
Stephen T C WongSystems Medicine and Bioengineering Department, Houston Methodist Cancer Center, Houston Methodist Hospital, Houston, United States.
Dingcheng GaoDepartment of Cardiothoracic Surgery, Weill Cornell Medicine, New York, United States.ORCID https://orcid.org/0000-0002-3903-2603

Funding

To study the EMT contributions in tumor metastasis and chemoresistance by using lineage tracing modelsR01CA244413 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI GAO, DINGCHENG · 2020 to 2024
$2.4M
Targeting the epithelial to mesenchymal transition-mediated chemoresistance in breast cancerR01CA205418 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI GAO, DINGCHENG · 2016 to 2020
$1.7M
NCI NIH HHS R01 CA205418NCI NIH HHS R01CA244413
6 · The paper itself

Abstract

Epithelial-to-mesenchymal transition (EMT) contributes significantly to chemotherapy resistance and remains a critical challenge in treating advanced breast cancer. The complexity of EMT, involving redundant pro-EMT signaling pathways and its paradox reversal process, mesenchymal-to-epithelial transition (MET), has hindered the development of effective treatments. In this study, we utilized a Tri-PyMT EMT lineage-tracing model in mice and single-cell RNA sequencing (scRNA-seq) to comprehensively analyze the EMT status of tumor cells. Our findings revealed elevated ribosome biogenesis (RiBi) during the transitioning phases of both EMT and MET processes. RiBi and its subsequent nascent protein synthesis mediated by ERK and mTOR signalings are essential for EMT/MET completion. Importantly, inhibiting excessive RiBi genetically or pharmacologically impaired the EMT/MET capability of tumor cells. Combining RiBi inhibition with chemotherapy drugs synergistically reduced metastatic outgrowth of epithelial and mesenchymal tumor cells under chemotherapies. Our study suggests that targeting the RiBi pathway presents a promising strategy for treating patients with advanced breast cancer.

Indexed as

Breast NeoplasmsDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionRibosomesAnimalsAntineoplastic AgentsCell Line, TumorFemaleHumansMiceOrganelle BiogenesisSignal TransductionAntineoplastic Agentsbreast cancercancer biologychemoresistanceEMThumanmouseribosome biogenesis

Identifiers

PMID39259576
PMCPMC11390108

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.