Format

Send to

Choose Destination
Sci Rep. 2019 Mar 22;9(1):5019. doi: 10.1038/s41598-019-41394-9.

≤ Cyclin D1 protein affecting global women's health by regulating HPV mediated adenocarcinoma of the uterine cervix.

Author information

1
Division of Molecular Genetics & Biochemistry, ICMR-National Institute of Cancer Prevention and Research (NICPR), Noida, India.
2
Division of Preventive Oncology, ICMR-National Institute of Cancer Prevention and Research (NICPR), Noida, India.
3
Department of Anatomy, VMMC & Safdarjung Hospital, New Delhi, India.
4
Division of Molecular Genetics & Biochemistry, ICMR-National Institute of Cancer Prevention and Research (NICPR), Noida, India. mausumi.bharadwaj@gmail.com.
5
Division of Preventive Oncology, ICMR-National Institute of Cancer Prevention and Research (NICPR), Noida, India. directornicpr@gmail.com.

Abstract

Adenocarcinoma (ADC) of the uterine cervix (UC) is a rare form of cervical cancer (CC) caused due to the infection of Human Papilloma Virus (HPV). Cyclin D1 is one of the downstream targets of aberrantly activated Notch signaling, contribute to the etiology of CC. However, little is known about the role of Cyclin D1 in the modulation of cervical ADC and is controversial. The purpose of this study is to determine the role of Cyclin D1 protein and to elucidate the combined analysis with Notch signaling proteins in HPV associated ADCs of CC. A total of 60 biopsy samples (40 normal and 20 ADCs of CC) were analyzed for the expression of Cyclin D1 in HPV associated ADCs via immunohistochemistry and by immunoblotting. HPV-16 positive ADC patients showed a strong association with the Cyclin D1 expression (p = 0.007). The significant mean difference (p = 0.0001) and the pairwise comparison between Cyclin D1/JAG1 (p = 0.0001), and Cyclin D1/Notch-3 (p = 0.0001) were observed. The above Notch signaling proteins showed their synergistic role in modulating Cyclin D1 which in-turn regulates HPV-16 associated ADC of the uterine cervix (UC), affecting women's global health.

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center