Evidence map›Paper›PMID 41348282›Full record

ArticleDiscover oncology2025

Lidocaine suppresses HER2-positive breast cancer cell proliferation by targeting the OGT-CCNL1 axis.

Yunfei Sun, Bo Liu, Xuan Zhang, Chengqi Deng, Nan Hu, Yiqing Yin

Abstract read
In one paragraph

Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

6 authors.

Yunfei Sun *Department of Anesthesiology, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin Medical University, Ministry of Education, Key Laboratory of Cancer Prevention and Therapy, West Huan-Hu Road, Ti Yuan Bei, Hexi District, Tianjin, China.
Bo Liu *Department of Clinical Laboratory, The Second Affiliated Hospital of Tianjin University of TCM, Tianjin, China.
Xuan ZhangDepartment of Anesthesiology, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin Medical University, Ministry of Education, Key Laboratory of Cancer Prevention and Therapy, West Huan-Hu Road, Ti Yuan Bei, Hexi District, Tianjin, China.
Chengqi DengDepartment of Anesthesiology, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin Medical University, Ministry of Education, Key Laboratory of Cancer Prevention and Therapy, West Huan-Hu Road, Ti Yuan Bei, Hexi District, Tianjin, China.
Nan HuDepartment of Anesthesiology, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin Medical University, Ministry of Education, Key Laboratory of Cancer Prevention and Therapy, West Huan-Hu Road, Ti Yuan Bei, Hexi District, Tianjin, China.
Yiqing YinDepartment of Anesthesiology, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin Medical University, Ministry of Education, Key Laboratory of Cancer Prevention and Therapy, West Huan-Hu Road, Ti Yuan Bei, Hexi District, Tianjin, China. yinyiqingdr@163.com.

Funding

National Natural Science Foundation of China No.82001479Tianjin Key Medical Discipline Construction Project Grant No.TJYXZDXK-3-003ATianjin Key Medical Discipline(Specialty) Construction Project TJYXZDXK-009A
6 · The paper itself

Abstract

backgroundHER2-positive breast cancer, known for its heterogeneity and complex molecular mechanisms, poses a significant therapeutic challenge. Lidocaine, a widely used local anesthetic, has recently been identified as a potential anticancer agent. This study investigates the effects of lidocaine on HER2-positive breast cancer proliferation and the underlying mechanisms.

methodsThe effects of lidocaine on cell proliferation, cell cycle distribution, and O-GlcNAcylation levels in AU565 and BT474 cells were assessed using CCK-8 assays, EdU incorporation assays, flow cytometry, and western blot analysis. Furthermore, the interaction between lidocaine and OGT was examined using molecular docking and co-immunoprecipitation (co-IP) experiments.

resultsLidocaine was found to significantly inhibit cell viability and proliferation in AU565 and BT474 cells, inducing G0/G1 cell cycle arrest. Mechanistically, lidocaine was observed to downregulate O-GlcNAc transferase (OGT), consequently reducing global O-GlcNAcylation levels. We further demonstrated that OGT interacts with and stabilizes CCNL1 via O-GlcNAcylation, and this interaction is critical for CCNL1-mediated cancer cell proliferation. Notably, rescue experiments revealed that the overexpression of either OGT or CCNL1 could partially reverse the suppressive effects of lidocaine.

conclusionsIn conclusion, this study reveals a novel mechanism by which lidocaine inhibits HER2-positive breast cancer cell proliferation by targeting the OGT-CCNL1 axis, highlighting a potential therapeutic avenue for HER2-positive breast cancer.

Indexed as

CCNL1HER2-positive breast cancerLidocaineO-GlcNAcylationOGTProliferation

Identifiers

PMID41348282
PMCPMC12796022

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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.