Estrogen upregulates DNA2 expression through the PI3K-AKT pathway in endometrial carcinoma.
- Author:
Xinyan WANG
1
;
Xiuling XU
2
;
Ting ZHANG
1
;
Yang JIN
2
;
Sheng XU
3
;
Lifeng CHEN
3
;
Yucheng LAI
3
;
Ling ZHANG
4
;
Ruolang PAN
5
;
Yan YU
6
Author Information
- Publication Type:Journal Article
- MeSH: Female; Humans; Proto-Oncogene Proteins c-akt; Phosphatidylinositol 3-Kinases; Endometrial Neoplasms; Estrogens; Breast Neoplasms; DNA Helicases
- From: Journal of Zhejiang University. Science. B 2023;24(3):262-268
- CountryChina
- Language:English
- Abstract: Endometrial cancer is the most common gynecological malignancy, affecting up to 3% of women at some point during their lifetime (Morice et al., 2016; Li and Wang, 2021). Based on the pathogenesis and biological behavioral characteristics, endometrial cancer can be divided into estrogen-dependent (I) and non-estrogen-dependent (II) types (Ulrich, 2011). Type I accounts for approximately 80% of cases, of which the majority are endometrioid carcinomas, and the remaining are mucinous adenocarcinomas (Setiawan et al., 2013). It is generally recognized that long-term stimulation by high estrogen levels with the lack of progesterone antagonism is the most important risk factor; meanwhile, there is no definite conclusion on the specific pathogenesis. The incidence of endometrial cancer has been on the rise during the past two decades (Constantine et al., 2019; Gao et al., 2022; Luo et al., 2022). Moreover, the development of assisted reproductive technology and antiprogestin therapy following breast cancer surgery has elevated the risk of developing type I endometrial cancer to a certain extent (Vassard et al., 2019). Therefore, investigating the influence of estrogen in type I endometrial cancer may provide novel concepts for risk assessment and adjuvant therapy, and at the same time, provide a basis for research on new drugs to treat endometrial cancer.
