Metabolic Landscape and Immune Microenvironment in Ovarian Cancer: Mechanisms of Remodelling and Therapeutic Opportunities

Ovarian Cancer (OC) is the most lethal gynaecological malignancy worldwide, with a 5-year survival rate of less than 50%. Most patients still face tumour recurrence and drug resistance, which is mainly attributed to its highly complex tumour immune microenvironment (TIME) and metabolic heterogeneity, where metabolic remodelling severely suppresses immune cell function. OC cells exhibit distinctive metabolic reprogramming during tumour development and progression. In addition, various cells such as tumour-associated macrophages and neutrophils collectively construct an immunosuppressive network through their respective metabolic pathways. In the hypoxic peritoneal niche, hypoxia-inducible factor-1α directly drives the expression of galectin-1 and intersects with the IDO1-kynurenine-AhR axis, jointly reinforcing regulatory T-cell expansion and T-cell exhaustion. Targeting metabolic reprogramming to reshape the TIME has become a research hotspot, and emerging strategies including the delivery of metabolic inhibitors via nanoplatforms have shown synergistic antitumour potential. This article elaborates the mechanisms of metabolic reprogramming between OC cells and various cell types within the TIME, focusing on breaking immune tolerance by correcting metabolic disorders, so as to provide theoretical support for novel therapeutic regimens for OC based on immunometabolic regulation.