Evidence map›Paper›PMID 41276477›Full record

ArticleJournal of Zhejiang University. Science. B2025

Selective anastasis induction by bee venom in normal cells: a promising strategy for breast cancer therapy with minimal impact on cell viability.

Sinan Tetikoglu, Muharrem Akcan, Ugur Uzuner, Selcen Celik Uzuner

Abstract read
In one paragraph

Article in Journal of Zhejiang University. Science. B, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

4 authors.

Sinan TetikogluDepartment of Molecular Biology and Genetics, Faculty of Science, Karadeniz Technical University, Trabzon 61080, Türkiye.
Muharrem AkcanDepartment of Biochemistry, Faculty of Arts and Sciences, Kütahya Dumlupınar University, Kütahya 43100, Türkiye.
Ugur UzunerDepartment of Molecular Biology and Genetics, Faculty of Science, Karadeniz Technical University, Trabzon 61080, Türkiye.
Selcen Celik UzunerDepartment of Molecular Biology and Genetics, Faculty of Science, Karadeniz Technical University, Trabzon 61080, Türkiye. selcen.celik@ktu.edu.tr.

Funding

the Karadeniz Technical University FBA-2018-7951 and FYL-2019-8116the Scientific and Technological Research Council of Türkiye (TUBITAK) 123Z002
6 · The paper itself

Abstract

Anastasis is a phenomenon described as a cellular escape from ethanol-induced cell death. Although the relevant mechanism has not yet been fully elucidated, anastasis is thought to play a role in drug resistance in cancer cells. To date, the regulation of anastasis in normal and cancerous cells has not been clarified. The current cancer treatment strategies are expected to selectively attack cancer cells without negatively affecting normal cell proliferation. Inspired by the anti-cancer potential of bee venom, this study is the first to evaluate whether bee venom has similar selectivity in producing an anastatic effect. The results indicated that bee venom induces anastasis in normal cells (Michigan Cancer Foundation-10A (MCF10A), Adult Retinal Pigment Epithelium cell line-19 (ARPE-19), and National Institutes of Health 3T3 cell line (NIH3T3)) but causes irreversible cell death in breast cancer cells (M.D. Anderson-Metastatic Breast-231 (MDA-MB-231) and Michigan Cancer Foundation-7 (MCF7)). Liver cancer (HepG2) cells were moderately more resistant to permanent cell death after bee venom treatment compared to breast cancer cells. However, cisplatin caused permanent non-selective cell death in both normal and cancerous cells. The selectivity indices after bee venom treatment were higher compared to cisplatin. Taken together, bee venom was shown to induce selective anastasis only in normal cells, not in cancer cells, which suggests that bee venom has significant potential in selective cancer therapy, especially for breast cancer, via promoting the recovery and maintenance of viability of normal cells.

Indexed as

Bee VenomsBreast NeoplasmsAnimalsAntineoplastic AgentsCell DeathCell Line, TumorCell SurvivalCisplatinFemaleHep G2 CellsHumansMCF-7 CellsMiceNIH 3T3 CellsAntineoplastic AgentsBee VenomsCisplatin

Identifiers

PMID41276477
PMCPMC12640745

What OpenQuestion holds

Textmetadata
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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.