ReviewDiscover oncology2025
KLF4 in cancer chemoresistance: molecular mechanisms and therapeutic implications.
Review in Discover oncology, 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.
- Comparative Molecular Insights and Computational Modeling of Multiple Myeloma and Osteosarcoma.International journal of molecular sciences · 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemoresistance is a major obstacle in cancer treatment, and it often results in treatment failure and disease progression. Among the plethora of factors contributing to chemoresistance, the transcription factor Krüppel-like factor 4 (KLF4) has emerged as a pivotal player. This review discusses the role of KLF4 in orchestrating various mechanisms underlying cancer chemoresistance. KLF4, originally identified as a regulator of cell differentiation and proliferation, has recently gained attention for its role in modulating cellular responses to chemotherapeutic agents. Through complex regulatory networks, KLF4 modulates the process of drug efflux, DNA repair, apoptotic signaling, tumor heterogeneity, and cancer cell stemness, leading to the development of cancer chemoresistance. Additionally, tissue or cell types specific post-translational modification (PTM) of KLF4 plays a significant role in the development of cancer chemoresistance. The review explores emerging possibilities and available information that can be utilised to understand the mechanism of chemoresistance mediated by KLF4 in cancer. In conclusion, understanding the complex mechanisms through which KLF4 orchestrates cancer chemoresistance opens promising avenues for developing more effective therapeutic interventions to combat treatment-resistant cancers.
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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.