Article3 Biotech2025
Targeting the interplay between human papillomavirus oncoproteins and hedgehog signaling: assessment of chemopreventive potential of carvacrol in cervical cancer.
Article in 3 Biotech, 2025. 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cervical carcinoma is the fourth most frequently diagnosed cancer and is a serious cause of increased mortality among females globally. Hedgehog/GLI signaling has now been established to play a pivotal role in imparting tumor recurrence and promoting metastasis in cervical carcinoma. HPV associated oncoproteins particularly E6/E7 concomitantly with altered signaling pathways are key determinants of cervical cancer. Nevertheless, the nexus between HPV oncogenes and Hedgehog/GLI signaling till date remains unclear. In this study, we investigated the anticancer and apoptotic potential of carvacrol against cervical cancer cells in vitro by targeting the plausible nexus between HPV oncoproteins and Hedgehog signaling. The findings from cell proliferation, LDH cytotoxicity, and morphology analysis suggested that carvacrol treatment significantly decreased the number of viable CaSki cells in a concentration and time-related manner. Morphological trademarks of cell death, including fragmentation of CaSki cell nucleus were studied by DAPI/PI and Hoechst33342 staining. The cytotoxicity of carvacrol was mediated through apoptosis, as confirmed by the Annexin V/FITC assay and caspase activation. Cell cycle analysis showed that carvacrol exerted significant impeding effects on the proliferation of CaSki cells via G
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