Tegaserod maleate exerts anti-tumor effects on prostate cancer via repressing sonic hedgehog signaling pathway

Prostate cancer (PCa) is a highly common type of malignancy and affects millions of men in the world since it is easy to recur or emerge therapy resistance. Therefore, it is urgent to find novel treatments for PCa patients. In the current study, we found that tegaserod maleate (TM), an FDA-approved agent, inhibited proliferation, colony formation, migration as well as invasion, caused the arrest of the cell cycle, and promoted apoptosis of PCa cells in vitro. In addition, TM suppressed the tumor growth in the cell-derived xenograft (CDX) mouse model in vivo. Mechanistically, TM exerted anti-tumor effects via downregulating GLI2, and its downtream targets, thus inhibiting the sonic hedgehog (SHH) signaling pathway. In brief, our findings demonstrated that TM effectively inhibited the activities of PCa cells by suppressing the SHH signaling pathway and provided a potential new agent for the treatment of PCa.

Authors

Institutions

Publication Details

Journal
Molecular Medicine
Published
2025-01-29
DOI
https://doi.org/10.1186/s10020-025-01080-1
Citations
1
Primary Topic
Hedgehog Signaling Pathway Studies
Type
article
Field-Weighted Citation Impact
0.81

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Tegaserod maleate exerts anti-tumor effects on prostate cancer via repressing sonic hedgehog signaling pathway

Shengdong Ge, Mingkun Chen, Donggen Zhong, Zhanghui Chen et al.
1 citations
Molecular Medicine
Hedgehog Signaling Pathway Studies
0.81
article

Tegaserod maleate exerts anti-tumor effects on prostate cancer via repressing sonic hedgehog signaling pathway

Shengdong Ge, Mingkun Chen, Donggen Zhong, Zhanghui Chen, Shan‐Chao Zhao, Yongcheng Ren, Ninghan Feng, Yaying Hong, Maoping Cai, Yao Chen, Yuan Liu, Zhe-Sheng Chen
article en
1 citations

Abstract

Prostate cancer (PCa) is a highly common type of malignancy and affects millions of men in the world since it is easy to recur or emerge therapy resistance. Therefore, it is urgent to find novel treatments for PCa patients. In the current study, we found that tegaserod maleate (TM), an FDA-approved agent, inhibited proliferation, colony formation, migration as well as invasion, caused the arrest of the cell cycle, and promoted apoptosis of PCa cells in vitro. In addition, TM suppressed the tumor growth in the cell-derived xenograft (CDX) mouse model in vivo. Mechanistically, TM exerted anti-tumor effects via downregulating GLI2, and its downtream targets, thus inhibiting the sonic hedgehog (SHH) signaling pathway. In brief, our findings demonstrated that TM effectively inhibited the activities of PCa cells by suppressing the SHH signaling pathway and provided a potential new agent for the treatment of PCa.

Molecular MedicineVol. 31(1)
Jiangnan University (CN), St. John's University (US), Third Affiliated Hospital of Southern Medical University (CN), Central People's Hospital of Zhanjiang (CN), Nanfang Hospital (CN), First Affiliated Hospital of Guangzhou University of Chinese Medicine (CN), Wuxi No.2 People's Hospital (CN), Wuxi People's Hospital (CN), Chinese People's Liberation Army (CN), Southern Medical University (CN), Nanjing Medical University (CN)
National Natural Science Foundation of China, Southern Medical University, National Key Research and Development Program of China, Basic and Applied Basic Research Foundation of Guangdong Province
Good health and well-being
Openalex Percentile: Top 31%
Hedgehog Signaling Pathway Studies
0.81
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.