STEAP3 promotes triple-negative breast cancer growth through the FGFR1-mediated activation of PI3K/AKT/mTOR signaling

Triple-negative breast cancer (TNBC) is a highly aggressive subtype with a poor prognosis and lacks effective targeted therapies. Six-transmembrane epithelial antigen of prostate 3(STEAP3) is specifically overexpressed in TNBC, but its precise role and molecular mechanisms remain unclear. Here, we show that STEAP3 is positively correlated with proliferation markers in TNBC, but not in non-TNBC. Further assays revealed that STEAP3 significantly enhances TNBC cell proliferation, invasion, and metastasis <i>in vitro</i>. Mechanistically, STEAP3 promotes TNBC progression by stabilizing FGFR1 and subsequently activating the PI3K/AKT/mTOR pathway. In xenograft models, STEAP3 knockdown suppressed tumor growth and reduced the expression of proliferation markers, consistent with <i>in vitro</i> findings. These results demonstrate STEAP3 as a key regulator of TNBC progression via FGFR1-mediated PI3K/AKT/mTOR signaling and highlight its potential as a promising therapeutic target.

Authors

Institutions

Publication Details

Journal
iScience
Published
2025-04-24
DOI
https://doi.org/10.1016/j.isci.2025.112526
Citations
3
Primary Topic
Fibroblast Growth Factor Research
Type
article
Field-Weighted Citation Impact
2.42

Funders

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

STEAP3 promotes triple-negative breast cancer growth through the FGFR1-mediated activation of PI3K/AKT/mTOR signaling

Lifang Yuan, Ping Sun, Junbao Liu, Yuhan Bao
3 citations
iScience
Fibroblast Growth Factor Research
2.42
article

STEAP3 promotes triple-negative breast cancer growth through the FGFR1-mediated activation of PI3K/AKT/mTOR signaling

Lifang Yuan, Ping Sun, Junbao Liu, Yuhan Bao
article en
3 citations

Abstract

Triple-negative breast cancer (TNBC) is a highly aggressive subtype with a poor prognosis and lacks effective targeted therapies. Six-transmembrane epithelial antigen of prostate 3(STEAP3) is specifically overexpressed in TNBC, but its precise role and molecular mechanisms remain unclear. Here, we show that STEAP3 is positively correlated with proliferation markers in TNBC, but not in non-TNBC. Further assays revealed that STEAP3 significantly enhances TNBC cell proliferation, invasion, and metastasis <i>in vitro</i>. Mechanistically, STEAP3 promotes TNBC progression by stabilizing FGFR1 and subsequently activating the PI3K/AKT/mTOR pathway. In xenograft models, STEAP3 knockdown suppressed tumor growth and reduced the expression of proliferation markers, consistent with <i>in vitro</i> findings. These results demonstrate STEAP3 as a key regulator of TNBC progression via FGFR1-mediated PI3K/AKT/mTOR signaling and highlight its potential as a promising therapeutic target.

iScienceVol. 28(6)
Yuhuangding Hospital (CN), Second Hospital of Shandong University (CN), Cancer Hospital of Huanxing Chaoyang District Beijing (CN)
Natural Science Foundation of Shandong Province, Wu Jieping Medical Foundation
Openalex Percentile: Top 12%
Fibroblast Growth Factor Research
2.42
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.

STEAP3 promotes triple-negative breast cancer growth through the FGFR1-mediated activation of PI3K/AKT/mTOR signaling — Lifang Yuan, Ping Sun, et al. · iScience (2025) | TGRS Research Map | TGRS