Evidence map›Paper›PMID 42365824›Full record

ArticleTranslational oncology2026

The YAP-TEAD4 inhibitor M511-0965 suppresses triple-negative breast cancer progression by downregulating TGFB2.

Mengxing Cheng, Xinyu Li, Na Song, Xinxia Yang, Xiaolei Ma, Haocheng Zhang, Yating Lei, Yanxin Jia, Lina Ba, Ruipu Zhang and 3 more

Abstract read
In one paragraph

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

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Mengxing ChengDepartment of Pharmacology (State Key Laboratory of Frigid Zone Cardiovascular Diseases, State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin 150086, China.
Xinyu LiDepartment of Pharmacology (State Key Laboratory of Frigid Zone Cardiovascular Diseases, State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin 150086, China.
Na SongDepartment of Pharmacology (State Key Laboratory of Frigid Zone Cardiovascular Diseases, State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin 150086, China.
Xinxia YangDepartment of Pharmacology (State Key Laboratory of Frigid Zone Cardiovascular Diseases, State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin 150086, China.
Xiaolei MaDepartment of Pharmacology (State Key Laboratory of Frigid Zone Cardiovascular Diseases, State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin 150086, China.
Haocheng ZhangDepartment of Pharmacology (State Key Laboratory of Frigid Zone Cardiovascular Diseases, State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin 150086, China; Department of Pharmacy, the Sixth Affiliated Hospital of Harbin Medical University, Harbin 150023, China.
Yating LeiDepartment of Pharmacology (State Key Laboratory of Frigid Zone Cardiovascular Diseases, State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin 150086, China.
Yanxin JiaDepartment of Pharmacology (State Key Laboratory of Frigid Zone Cardiovascular Diseases, State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin 150086, China.
Lina BaDepartment of Pharmacology (State Key Laboratory of Frigid Zone Cardiovascular Diseases, State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin 150086, China.
Ruipu ZhangDepartment of Orthopedics, the Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Lidan BaiDepartment of Orthopedics, the Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Wenxiao XuDepartment of Orthopedics, the Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China. Electronic address: wenxuhmu@outlook.com.
Guofen QiaoDepartment of Pharmacology (State Key Laboratory of Frigid Zone Cardiovascular Diseases, State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin 150086, China. Electronic address: qiaogf@hrbmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) lacks standard targeted therapies, and chemotherapy is associated with significant side effects and economic burden, highlighting the urgent need to develop novel low-toxicity and low-cost strategies. The Hippo pathway serves as a critical regulator of organ development. Its activation phosphorylates Yes-associated protein (YAP) and transcriptional coactivator TAZ, promoting their cytoplasmic degradation and inhibiting their binding to the nuclear transcription factor TEAD, thereby suppressing downstream gene expression. As the terminal effector of this pathway, TEAD plays an important role in various tumors. In this study, bioinformatics and molecular biology experiments revealed that TEAD4 is highly expressed in TNBC, and its expression level influences the biological functions of TNBC. Thus, TEAD4 represents an important therapeutic target for tumors, underscoring the need to identify safe and low-toxicity TEAD4 small-molecule inhibitors. Structure-based virtual screening has become a key step in drug discovery. Focusing on the crystal structure of the YAP/TEAD4 complex, we employed molecular docking technology for screening and identified a novel small-molecule inhibitor. Molecular biology and cellular functional assays confirmed that this inhibitor acts by targeting the YAP/TEAD4 interaction, thereby exerting antitumor effects. This preclinical study provides new insights and experimental evidence for targeted therapy in TNBC.

Indexed as

M511-0965Small molecule inhibitorTEAD4TGFB2TNBCVirtual screening

Identifiers

PMID42365824
PMCPMC13321392

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.