ArticleMedical oncology (Northwood, London, England)2025
Investigating the impact of berberine on autophagy-mediated drug resistance in chronic lymphocytic leukemia tumor cells.
Article in Medical oncology (Northwood, London, England), 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.
- Cellular and Molecular Mechanisms of Berberine in Cancer Therapy: Recent Advances.Archiv der Pharmazie · 2026Review
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
The persistence of drug resistance and relapses post-remission in B-chronic lymphocytic leukemia (B-CLL) underscores the exploration of novel therapeutic interventions. Given the pivotal role of autophagy in cancer cell resistance to apoptosis, this study aims to investigate the therapeutic potential of Berberine in modulating autophagy function associated with drug resistance in B-CLL. Peripheral blood mononuclear cells (PBMCs) from 10 CLL patients and 5 healthy individuals were treated with Berberine and Idelalisib (as a control). Flow cytometry analysis was employed to assess the protein expression levels of Beclin1, indicative of autophagy function, and high mobility group protein 1 (HMGB1), serving as an internal control for drug resistance. Furthermore, qRT-PCR was utilized to measure the expression levels of drug resistance markers including Beclin1, HMGB1, heat shock factor binding protein 1 (HSBP1), and receptor for advanced glycation end products (RAGE). Our findings revealed that Berberine exhibited a dual suppressive effect on Beclin1 and HMGB1 levels compared to the control drug. Moreover, Berberine downregulated the expression of the primary HMGB1 receptor, RAGE, in PBMCs from CLL patients. Notably, no significant alteration was observed in HSBP1 expression, a mediator of autophagy induction, upon Berberine treatment. These findings suggest that Berberine may target specific mechanisms associated with autophagy-mediated drug resistance, underscoring its therapeutic potential in B-CLL. Further clinical trials are warranted to validate the therapeutic efficacy of Berberine in B-CLL.
Indexed as
Identifiers
40473844What 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.