ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Oroxylin A exerts antiproliferative effects through downregulation of E6 and E7 oncogenes in cervical cancer HeLa cells.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- Review
- Metabolomics as a tool for understanding and treating triple-negative breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Numerous plant compounds have shown promising antitumor potential against cervical cancer. Plant-based compounds offer abundantly available, easy, and inexpensive methods of treatment over genome-editing technologies (immunotherapeutics). Many flavonoids directly abrogated HPV-E6/E7 activity with a concomitant apoptotic conclusion. Cervical cancer initiation and progression are entirely dependent on the oncogenes E6 and E7 (constitutively expressed) leading to tumorigenesis. Therefore, the manipulation of these oncogenes is the most prominent form of cervical cancer therapeutics. To further explore the mechanism underlying apoptosis induction, ROS generation, apoptosis-related gene expression (Bcl-2, caspases-3, caspases-8, and caspases-9), viral oncogenes (E6/E7), and tumor suppressor proteins (p53/pRb) were evaluated using MTT, cell cycle arrest, Hoechst, docking, and RT-PCR analysis. This study showed that oroxylin A (OrA) effectively inhibited HeLa cell proliferation at the respective doses. This study suggests that OrA inhibits E6/E7 mRNAs, leading to the upregulation of p53/pRb (tumor suppressor genes) in HeLa cells. Moreover, OrA induced p53-mediated apoptosis induction, activating the transcription of various proapoptotic genes, including Bcl-2 and Bax. Alternatively, p53 triggers apoptosis by promoting the caspase activation. In conclusion, OrA targeting E6/E7 was highly effective in inhibiting cancer cell proliferation via the upregulation of suppressor genes in cervical cancer.
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Identifiers
41032091What Socratic 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 Socratic graph.