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PKCδVIII and Bcl2 Increase Ovarian Cancer Survival via LncRNA NEAT1 Secreted by Obese Adipose Derived Stem Cells

Ovarian cancer remains the most common cause of death from gynecologic malignancy in US. The impact of obesity on the incidence and treatment of gynecologic cancer is growing in importance. Little is known about the molecular factors obesity imparts to the cancer niche that account for this relationship. Adipose‐derived stem cells (ADSC) can be isolated from stromal vascular fraction of abdominal white adipose tissue. We isolated and differentiated ADSC into adipocytes and previously showed that ADSC derived from lean and obese patients have distinct differences in gene expression. We evaluated the possibility that the secretome of obese ADSC could have paracrine effects on ovarian cells promoting growth and development of cancer cells. We show that NEAT1 levels secreted by ADSC from obese patients (ADSCo) were considerably higher than from normal ADSC both in cells and its secretome. Ovarian cancer high mortality rates are further exacerbated by cisplatin‐resistant cancers. Our data shows cisplatin‐resistant ovarian cells TOV‐112D cells had 5–fold higher expression of the survival protein Bcl2, and 10‐fold higher PKCδVIII, a signaling kinase which upregulates expression of Bcl2. Further, NEAT1 secreted from ADSCo increases Bcl2 and PKCδVIII expression. Cell proliferation assays and migration assays indicated that ADSCo‐CM increase TOV112D tumor cell migration. When ADSC NEAT1 was silenced, tumor cell migration decreased. These results indicate that the deleterious paracrine effects of genetically modified ADSC from obese patients may contribute to the poorer oncologic outcomes of ovarian cancer.