Evidence map›Paper›PMID 42141178›Full record

ArticleJournal of molecular histology2026

Study on the synergistic efficacy and mechanism of CD24 silencing combined with trastuzumab in HER2-positive breast cancer.

Yi Lu, Xinglu Zhou, Yue Gao, Zi Zhu, Bao Deng, Wubin Lv, Zhenkun Fu, He Ding, Lei Zhong

Abstract read
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In one paragraph

Article in Journal of molecular histology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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.

Yi Lu *Department of Breast Surgery, Sixth Affiliated Hospital of Harbin Medical University, No. 998 Aiying Street, Songbei District, Harbin City, 150023, Heilongjiang, China.
Xinglu Zhou *Department of PET/CT Center, Harbin Medical University Cancer Hospital, No. 150 Haping Road, Nangang District, Harbin City, China.
Yue GaoDepartment of Breast Surgery, Sixth Affiliated Hospital of Harbin Medical University, No. 998 Aiying Street, Songbei District, Harbin City, 150023, Heilongjiang, China.
Zi ZhuDepartment of Breast Surgery, Sixth Affiliated Hospital of Harbin Medical University, No. 998 Aiying Street, Songbei District, Harbin City, 150023, Heilongjiang, China.
Bao DengDepartment of Breast Surgery, Sixth Affiliated Hospital of Harbin Medical University, No. 998 Aiying Street, Songbei District, Harbin City, 150023, Heilongjiang, China.
Wubin LvKey Laboratory of Superlight Materials and Surface Technology, College of Materials Science and Chemical Engineering, Ministry of Education, Harbin Engineering University, Harbin, China.
Zhenkun FuDepartment of Immunology, School of Basic Medical Sciences, Harbin Medical University, No. 157 Baojian Street, Nangang District, Harbin City, China. 300042@hrbmu.edu.cn.
He DingKey Laboratory of Superlight Materials and Surface Technology, College of Materials Science and Chemical Engineering, Ministry of Education, Harbin Engineering University, Harbin, China. dinghe@hrbeu.edu.cn.
Lei ZhongDepartment of Breast Surgery, Sixth Affiliated Hospital of Harbin Medical University, No. 998 Aiying Street, Songbei District, Harbin City, 150023, Heilongjiang, China. zhonglei@hrbmu.edu.cn.

Funding

Clinical Research of Chen Jumei Foundation Z2025040110National Natural Science Foundation of China No. 52272273Natural Science Foundation of Heilongjiang Province of China PL2024H153
6 · The paper itself

Abstract

purposeReduced response to targeted therapy in human epidermal growth factor receptor 2 (HER2)-positive breast cancer underscores the need for novel therapeutic strategies and molecular targets. Cluster of differentiation 24 (CD24), an oncogenic molecule closely associated with aggressive tumor phenotypes, was investigated for its expression in HER2-positive breast cancer and its potential as a candidate target for combination therapy.

methodsHerein, we explored the expression of CD24 in breast cancer (BC) and its prognostic significance. In HER2-positive BC cells, CD24 was knocked down to assess its impacts on tumor biological behaviors and synergistic effects with trastuzumab. Furthermore, the underlying mechanism of CD24 was elucidated using a series of experimental assays, including Western blotting (WB), immunohistochemistry (IHC), terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay, and mRFP-GFP-LC3 dual-fluorescence autophagy assay. In vivo experiments were conducted to evaluate the therapeutic efficacy of CD24 inhibition combined with trastuzumab.

resultsCD24 was highly expressed in HER2 + breast cancer and associated with poor prognosis. CD24 knockdown significantly suppressed the proliferation, migration, and invasion of HER2-positive BC cells. Moreover, CD24 depletion promoted apoptosis and autophagy in HER2-positive breast cancer, accompanied by the inactivation of the Akt/mammalian target of rapamycin (mTOR) signaling pathway. In vivo data demonstrated that the combination regimen of CD24 knockdown and trastuzumab markedly reduced tumor burden.

conclusionCD24 silencing modulates autophagy and induces apoptosis via Akt/mTOR inhibition, and its combination with trastuzumab exerts potent antitumor effects, offering a promising strategy for HER2 + breast cancer.

Indexed as

Breast NeoplasmsCD24 AntigenErb-b2 Receptor Tyrosine KinasesGene SilencingTrastuzumabAnimalsApoptosisAutophagyCell Line, TumorCell MovementCell ProliferationFemaleHumansMiceSignal TransductionTOR Serine-Threonine KinasesCD24 AntigenCD24 protein, humanERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesTOR Serine-Threonine KinasesTrastuzumabApoptosisAutophagyCD24HER2-positive breast cancerTrastuzumab

Identifiers

PMID42141178

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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.