ArticlePloS one2026
Ivermectin inhibits ER, HER2, and TGF-β pathways in ER-positive and endocrine-resistant breast cancer cells.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ivermectin (IVM), initially developed as an antiparasitic drug, has recently demonstrated notable anticancer activity in several malignancies, including breast cancer. Our previous work showed that IVM inhibited cell proliferation and invasion in breast cancer cells, primarily through modulation of the Wnt signaling pathway. Preliminary results further indicated that combining IVM with tamoxifen enhanced its antiproliferative effects in endocrine-resistant breast cancer cells, suggesting a potential role in overcoming drug resistance. To further clarify IVM's mechanism in the context of endocrine resistance, this study investigated its effects on estrogen receptor-positive (ER⁺) and endocrine-resistant breast cancer cells. IVM significantly suppressed estrogen-induced proliferation and downregulated key resistance-associated markers, including ER and HER2. Additionally, IVM treatment markedly reduced ERK, a downstream effector linked to HER2 and TGF-β signaling. This inhibition was accompanied by a decrease in phosphorylated SMAD2 (pSMAD2) within the TGF-β pathway, while levels of SMAD4-a factor associated with favorable prognosis in endocrine resistance-were maintained. Collectively, these findings highlight IVM's potential as a repurposed therapeutic agent, with the dual capacity to prevent endocrine resistance in ER⁺ breast cancer and to enhance anti-hormonal therapies in resistant cases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.