ArticleBMC cancer2025
ACTC1 promotes tumor progression by upregulating BMP4 expression in prostate cancer.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer (PRAD) is a major malignancy affecting men worldwide. In this study, integrative analysis of public datasets and immunohistochemistry revealed that ACTC1 is upregulated in PRAD. Functional assays showed that ACTC1 overexpression promoted cell proliferation and migration, while its knockdown suppressed malignant behaviors. Consistently, xenograft experiments confirmed that ACTC1 enhanced tumor growth in vivo. Transcriptomic and pathway analyses indicated that ACTC1 regulates immune and inflammatory signaling, with BMP4 identified as a key downstream effector. Moreover, BMP4 overexpression rescued the inhibitory effects of ACTC1 knockdown on proliferation and migration, indicating that ACTC1 drives tumor progression through the BMP4 pathway. Together, our results identify ACTC1 as an oncogenic regulator of prostate cancer progression and suggest the ACTC1–BMP4 axis as a potential therapeutic target.
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Registered trials
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