Improving Treatment Strategies Research for Endometrial Cancer

The Endometrium and Endometrial Cancer

The endometrium is a layer of epithelial cells that lines the uterus and is where implantation of an embryo occurs and where the placenta of a growing fetus will develop. The female reproductive system is tightly controlled by the cycling of hormones, which also regulate the behavior of the endometrium. Every month in preparation for implantation of an embryo, the endometrium thickens; in the absence of an embryo, the thickened endometrium is shed in the process of menstruation. Additionally, endometrial dysfunction can lead to serious conditions like endometriosis, which can cause chronic pelvic pain and infertility.

Endometrial cancer is the most common cancer of the female reproductive tract in the United States, with over 65,000 cases estimated to be diagnosed this year and over 12,000 endometrial-related deaths.

Check out the Lifeline® catalog for our normal endometrial epithelial cells and other female reproductive cell systems, including:

• Human uterine smooth muscle cells
• Fallopian tube epithelial cells
• Vaginal epithelial cells
• Endometrial (uterine) epithelial cells
• Uterine fibroblasts
• Cervical Epithelial cells

Lifeline Endometrial Epithelial Cells as Normal Controls in Cancer Research

The five-year survival rate (opens in new window) for patients with endometrial cancer with localized spread is 95%, while for those with distant spread, the five-year survival rate is 17%. To improve current treatment strategies, a better understanding of the pathogenesis of the disease is needed. In particular, eukaryotic initiation factor 3 subunit B (EIF3B), a subunit of the EIF3 translation initiation factor, has been implicated as a tumor-promoting factor in a number of cancer types. In a 2019 study, Min and Chen (opens in new window) set out to determine whether EIF3B plays a role in the pathogenesis of endometrial cancer.

First, the authors examined EIF3B mRNA expression in the endometrial cancer cell lines Ishikawa, HEC-1A, RL95-2, and EFE-184. Using Lifeline normal endometrial epithelial cells grown in ReproLife™ medium as normal non-cancerous controls, the authors found that EIF3B mRNA levels were significantly increased in three of the four endometrial cancer cell lines (Ishikawa, HEC-1A, and RL95-2 cell lines).

To determine how the loss of EIF3B affects endometrial cancer cell behavior, the authors reduced the levels of EIF3B in HEC-1A cells (the cell line with the highest EIF3B levels) using siRNA. Compared with HEC-1A cells transfected with a control siRNA, HEC-1A cells with reduced EIF3B expression exhibited decreased proliferation, and an increased rate of apoptosis.

Additionally, the researchers demonstrated that HEC-1A cells with reduced EIF3B expression had lower rates of migration and invasion compared with HEC-1A cells with intact EIF3B. Finally, the group showed that reduction of EIF3B in HEC-1A cells was associated with lower levels of b-catenin (CTNNB1) mRNA, as well as decreased levels of CCNE1 (Cyclin E1), a downstream target of b-catenin signaling. As b-catenin is an established oncogene for multiple cancer types, the authors suggested that the effects of EIF3B on cancer-inducing endometrial cell behavior may be mediated by the b-catenin signaling pathway.

Together, the results of this study demonstrate that EIF3 is increased in some endometrial cell lines, where it contributes to cancer-promoting behavior, including increasing proliferation and inhibiting apoptosis.

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Endometrial cancer statistics and survival rates from www.cancer.org.