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Adiposity tied to increased progression of endometrial cancer, study finds
USA: Results from a recent study in the journal Gynecologic Oncology suggest that increased adiposity is a likely contributor to accelerated endometrial cancer (EC) growth and proliferation. Further, the intratumoral and paracrine adipose environments were found to have EC cell growth and proliferation. Also, there was a presence of endocrine effects but were sporadic with less impact on...
USA: Results from a recent study in the journal Gynecologic Oncology suggest that increased adiposity is a likely contributor to accelerated endometrial cancer (EC) growth and proliferation. Further, the intratumoral and paracrine adipose environments were found to have EC cell growth and proliferation. Also, there was a presence of endocrine effects but were sporadic with less impact on the tumorigenic pathways studied.
The annual incidence of endometrial cancer (EC) is estimated to increase by1–2%. Currently, more than half of all endometrioid EC diagnoses are attributable to obesity -- an independent risk factor for EC. Multiple epidemiologic studies have shown that obesity significantly increases the risk of several cancer types, however, there is no clarity on the mechanisms by which obesity contributes to EC progression.
Considering the above, Logan Blankenship, UT Health Science Center, San Antonio, and colleagues aimed to compare the effects of adiposity on endometrioid endometrial cancer cells in a paracrine, endocrine, and intratumoral environment both in-vitro and in vivo.
For this purpose, the researchers collected all patient samples, EC tissue, serum, and adipose tissue through the institutional tumor registry under IRB approval. For a paracrine-like environment representation, primary EC tissue-derived cells and established EC cell lines were treated with primary adipocyte conditioned medium (ADP-CM) and co-cultured together in a communicating chamber (co-culture assay). By culturing primary and established EC cells in low vs. high BMI patient serum, the endocrine effect was mimicked.
The effect of adiposity on EC cells was determined. Using RNA-seq, Western blotting, RT-qPCR, and reporter assays, mechanistic studies were conducted. To look at the effect of the tumor microenvironment in vivo, xenograft models were used in which cancer cells were co-implanted with or without adipocytes.
Following were the salient findings of the study:
- Treatment of established and primary EC cells with ADP-CM, co-culture, and stimulation with high BMI patient serum increased EC proliferation, long-term colony formation, and growth of EC organoid models.
- Mechanistic studies showed that all three environments also enhanced the expression of several oncogenic signaling pathways including STAT3, mTOR, Akt, and MAPK in EC cells.
- RNA-seq studies showed that ADP-CM treatment significantly altered the expression of 209 genes compared to control.
- Gene set enrichment (GSEA) analysis showed that ADP-CM regulated genes positively correlated with cytokine and STAT3 mediated signaling pathways, stem cells, inflammation, TGFβ, and interferon signaling pathways.
- In xenograft assays using SCID mice, co-implantation of EC cells with adipose cells significantly enhanced EC tumor growth in vivo.
"The findings can help to focus future study on pathways affected by visceral adipose at the tumoral level in obese patients to find new targets for future therapies," the authors concluded.
The study titled, "The role of adiposity in endometrioid endometrial cancer," was published in the journal Gynecologic Oncology.
Medha Baranwal joined Medical Dialogues as an Editor in 2018 for Speciality Medical Dialogues. She covers several medical specialties including Cardiac Sciences, Dentistry, Diabetes and Endo, Diagnostics, ENT, Gastroenterology, Neurosciences, and Radiology. She has completed her Bachelors in Biomedical Sciences from DU and then pursued Masters in Biotechnology from Amity University. She has a working experience of 5 years in the field of medical research writing, scientific writing, content writing, and content management. She can be contacted at email@example.com. Contact no. 011-43720751