ArticleScientific reports2018
Jagged-1 induced molecular alterations in HPV associated invasive squamous cell and adenocarcinoma of the human uterine cervix.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Review
- Review
- ≤ Cyclin D1 protein affecting global women's health by regulating HPV mediated adenocarcinoma of the uterine cervix.Scientific reports · 2019Article
- HES1 Protein Modulates Human Papillomavirus-Mediated Carcinoma of the Uterine Cervix.Journal of global oncology · 2019Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The majority of cervical cancer (CC) cases are attributable to HPV infection. Altered Notch pathway signals and HPV are believed to modify clinicopathogenesis of CC, however, the involvement of each molecular player and its mechanism is still not known. Jagged-1 (JAG1) is one of the ligands that induce Notch pathway. The involvement of JAG1 in the modulation of a disease condition is not very clear. Hence, this study aims to study the role of JAG1 in HPV-16/18 associated different histological sub-types of CC, especially ADC. 40 non-neoplastic cervical tissues, 30 precancer and 118 tumor specimens (total 188 tissue biopsies) were studied for the expression of the JAG1 protein through immunohistochemistry, immunoblotting and for HPV infection. Two folds increase of cytoplasmic (Mean ± S.E, 3.67 ± 0.33; p = 0.0001) and nuclear (3.70 ± 0.38, p = 0.0001) JAG1 expression was identified in normal (N) vs precancer and three folds cytoplasmic (4.44 ± 0.17, p = 0.0001) and nuclear (4.64 ± 0.17; p = 0.0001) in N vs. ISCC. Total 85% of ADC patients were found to be infected with HPV, which were 100% infected with HPV-16. These findings suggest the complex synergistic interplay between JAG1 and HPV in regulating clinicopathological progression of CC through its deregulation.
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