BACKGROUND Our previous study showed that human omental adipose-derived stem cells (ADSCs) promote ovarian cancer growth and metastasis. In this study, the role of autophagy in the ovarian cancer-promoting effects of omental ADSCs was further determined. METHODS The growth and invasion of ovarian cancer cells were detected by CCK-8 and Transwell assays, respectively. The autophagy of ovarian cancer cells transfected with MRFP-GFP-LC3 adenoviral vectors was evaluated by confocal microscopy and western blot assay. Transfection of STAT3 siRNA was used to inhibit the expression of STAT3. RESULTS Our results show that autophagy plays a vital role in ovarian cancer and is promoted by ADSCs. Specifically, we show that proliferation and invasion are correlated with autophagy induction by ADSCs in two ovarian cancer cell lines under hypoxic conditions. Mechanistically, ADSCs activate the STAT3 signalling pathway, thereby promoting autophagy. Knockdown of STAT3 expression using siRNA decreased hypoxia-induced autophagy and decreased the proliferation and metastasis of ovarian cancer cells. CONCLUSION Taken together, our data indicate that STAT3-mediated autophagy induced by ADSCs promotes ovarian cancer growth and metastasis.

中文翻译：

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人网膜脂肪来源的间充质干细胞通过STAT3信号通路增强卵巢癌细胞的自噬能力。

背景技术我们先前的研究表明，人类网膜脂肪干细胞（ADSCs）促进卵巢癌的生长和转移。在这项研究中，进一步确定了自噬在网膜ADSCs促进卵巢癌的作用中的作用。方法分别用CCK-8和Transwell法检测卵巢癌细胞的生长和侵袭能力。通过共聚焦显微镜和蛋白质印迹分析评估了用MRFP-GFP-LC3腺病毒载体转染的卵巢癌细胞的自噬。STAT3 siRNA的转染用于抑制STAT3的表达。结果我们的结果表明自噬在卵巢癌中起着至关重要的作用，并由ADSC促进。具体而言，我们表明在缺氧条件下，两个卵巢癌细胞系中ADSCs的增殖和侵袭与ADSCs自噬诱导相关。从机制上讲，ADSC激活STAT3信号通路，从而促进自噬。使用siRNA抑制STAT3表达可减少缺氧诱导的自噬，并降低卵巢癌细胞的增殖和转移。结论综上所述，我们的数据表明ADSCs诱导的STAT3介导的自噬促进卵巢癌的生长和转移。