ArticleMolecular biology reports2025
Zataria multiflora extract enhances imatinib-induced cytotoxicity in chronic myeloid leukemia and multiple myeloma cells.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Methanolic extract of Zataria multiflora and arsenic trioxide combination therapy modulates oncogenic and tumor suppressor MicroRNA expression and RAF1 signaling in NB4 acute promyelocytic leukemia cells.Medical oncology (Northwood, London, England) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundZataria multiflora (ZM) is a medicinal plant with widespread antitumor effects. Tyrosine kinase inhibitors (TKIs) are considered the mainstay treatment in blood cancers; however, eventual resistance to TKIs poses a significant challenge in this area. The present study aimed to assess the synergistic effects of ZM extract (ZME) along with imatinib, a TKI, against K-562 and U-266 leukemic cell lines.
methodsCell viability was evaluated using the MTT assay, and apoptosis assessment was also conducted through Annexin-V/PI staining. Additionally, Real-Time PCR was used to assess the expression levels of BCR-ABL, P-TEN, c-MYC, Bax, and Bcl-2 genes. Molecular docking was carried out as an in-silico technique for both BCL-2 and ABL proteins.
resultsThe results showed that both ZME and imatinib promoted apoptosis in K562 and U266 cells, with combination treatment significantly enhancing apoptotic cell death (e.g., 18.4% apoptosis in K562 cells with ZME + imatinib vs. 8.5% untreated; 46.9% in U266 cells vs. 11.6% untreated, P < 0.05). Combined treatment with imatinib and ZME upregulated the expression of Bax (5-fold in K562, 3-fold in U266) and P-TEN (2-fold in K562, 2.8-fold in U266) genes and downregulated the expression of Bcl-2 (0.3-fold in K562, 0.3-fold in U266), BCR-ABL (0.5-fold in K562), and c-MYC (0.4-fold in K562, 0.2-fold in U266) genes (P < 0.05). Molecular docking showed strong binding affinities between ZME constituents (carvacrol and thymol) and BCL-2 and ABL proteins.
conclusionsZME shows potential as a complementary agent in vitro, warranting further investigation.
Indexed as
Identifiers
41085796What 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.