Evidence map›Paper›PMID 42210419›Full record

ArticleCell & bioscience2026

Cannabidiol enhances tamoxifen efficacy via CREB-mediated suppression of ERα signaling in ER-positive breast cancer cells.

Bu Gyeom Kim, Okhyeon Kim, Do-Yeon Lee, Bo Ram Kim, Dae Yeong Kim, Yoon Namgung, Jun Woo Bong, Sanghee Kang, Sun Il Lee, Sang Cheul Oh

Abstract read
In one paragraph

Article in Cell & bioscience, 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

10 authors.

Bu Gyeom KimDepartment of Oncology, Korea University Guro Hospital, Korea University College of Medicine, 08308, Seoul, Republic of Korea.
Okhyeon KimDepartment of Oncology, Korea University Guro Hospital, Korea University College of Medicine, 08308, Seoul, Republic of Korea.
Do-Yeon LeeDepartment of Oncology, Korea University Guro Hospital, Korea University College of Medicine, 08308, Seoul, Republic of Korea.
Bo Ram KimDepartment of Oncology, Korea University Guro Hospital, Korea University College of Medicine, 08308, Seoul, Republic of Korea.
Dae Yeong KimDepartment of Oncology, Korea University Guro Hospital, Korea University College of Medicine, 08308, Seoul, Republic of Korea.
Yoon NamgungDepartment of Oncology, Korea University Guro Hospital, Korea University College of Medicine, 08308, Seoul, Republic of Korea.
Jun Woo BongDepartment of Surgery, Korea University Guro Hospital, Korea University College of Medicine, 08308, Seoul, Republic of Korea.
Sanghee KangInstitute of Convergence New Drug Development, Korea University College of Medicine, Seoul, 02841, Republic of Korea.
Sun Il LeeInstitute of Convergence New Drug Development, Korea University College of Medicine, Seoul, 02841, Republic of Korea.
Sang Cheul OhDepartment of Oncology, Korea University Guro Hospital, Korea University College of Medicine, 08308, Seoul, Republic of Korea. sachoh@korea.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEstrogen receptor alpha (ERα) plays a crucial role in the proliferation and survival of ER-positive breast cancer cells, and tamoxifen (TAM) remains the mainstay of endocrine therapy. However, acquired resistance to TAM remains a major clinical challenge. Despite advances in molecular profiling and targeted therapies, the mechanisms underlying TAM resistance remain incompletely understood. Emerging evidence suggest that dysregulation of intracellular signaling pathways, including the cAMP/CREB axis, may contribute to endocrine therapy failure.

methodsWe investigated the effects of cannabidiol (CBD) on TAM sensitivity and elucidated its underlying mechanisms in ER-positive breast cancer models. Human breast cancer cell lines (MCF7 and T47D) were treated with CBD, TAM or their combination. Apoptosis, proliferation, and protein expression were evaluated by flow cytometry, western blotting, and immunofluorescence. In vivo efficacy was examined in xenograft models.

resultsCBD significantly enhanced TAM-induced cell death and apoptosis in ER-positive breast cancer cell. Mechanistically, CBD suppressed the cAMP/CREB signaling pathway, leading to downregulation of ERα and its target genes (TFF1, GREB1, CCND1). Co-immunoprecipitation revealed that CBD inhibited the interaction between phosphorylated CREB and CBP, resulting in transcriptional suppression of ERα. In vivo, combined treatment with CBD and TAM synergistically inhibited tumor growth and reduced ERα and p-CREB expression levels in tumor tissues.

conclusionsOur findings demonstrate that CBD restores TAM sensitivity through CREB-mediated downregulation of ERα signaling in ER-positive breast cancer. This study suggests the potential application of CBD as a novel adjuvant agent to overcome TAM resistance and improve therapeutic outcomes in patients with ER-positive breast cancer.

Identifiers

PMID42210419
PMCPMC13411534

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.