Ovarian carcinoma is the deadliest type of gynecological cancer. The unique tumor microenvironment enables specific and efficient metastasis, weakens immunological monitoring, and mediates drug resistance. Tumor associated macrophages (TAMs) are a crucial part of the TME and are involved in various aspects of tumor behavior. Lysophosphatidic acid (LPA) is elevated in the blood of ovarian carcinoma patients, as well as in the tumor tissues and ascites, which make it a useful biomarker and a potential therapeutic target. Recent studies have shown that LPA transforms monocytes into macrophages and regulates the formation of macrophages through the AKT/mTOR pathway, and PPAR γ is a major regulator of LPA-derived macrophages. In addition, TAMs synthesize and secrete LPA and express LPA receptor (LPAR) on the surface. With these data in mind, we hypothesize that LPA can convert monocytes directly into TAMs in the microenvironment of ovarian cancer. LPA may mediate TAM formation by activating the PI3K/AKT/mTOR signaling pathway through LPAR on the cell surface, which may also affect the function of PPAR γ, leading to increased LPA production by TAMs. Thus, LPA and TAMs form a vicious circle that affects the malignant behavior of ovarian cancer.

中文翻译：

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溶血磷脂酸与卵巢癌中肿瘤相关巨噬细胞之间的潜在相互作用。

卵巢癌是最致命的妇科癌症。独特的肿瘤微环境可实现特定而有效的转移，削弱免疫学监测并介导耐药性。肿瘤相关巨噬细胞（TAM）是TME的重要组成部分，涉及肿瘤行为的各个方面。溶血磷脂酸（LPA）在卵巢癌患者的血液以及肿瘤组织和腹水中升高，这使其成为有用的生物标记物和潜在的治疗靶标。最近的研究表明，LPA通过AKT / mTOR途径将单核细胞转化为巨噬细胞并调节巨噬细胞的形成，而PPARγ是LPA衍生巨噬细胞的主要调节剂。另外，TAM合成并分泌LPA，并在表面表达LPA受体（LPAR）。考虑到这些数据，我们假设LPA可以在卵巢癌的微环境中将单核细胞直接转化为TAM。LPA可能通过激活细胞表面LPAR上的PI3K / AKT / mTOR信号通路来介导TAM的形成，这也可能影响PPARγ的功能，从而导致TAM产生LPA的增加。因此，LPA和TAM形成恶性循环，影响卵巢癌的恶性行为。