Autonomous driving paper index
Sex as a Biological Determinant of the Warburg Effect: A Narrative Review of Hormonal, Chromosomal, and Epigenetic Mechanisms in Cancer
One-line summary
Background and Rationale Sex differences in cancer incidence, progression, and mortality are well documented across multiple cancer types, yet the molecular mechanisms driving these disparities remain incompletely characterised.
Engineering notes
Key topics: autonomous driving, control. See the paper for implementation details and experimental results.
Chinese explanation / 中文解读
中文解读待补充：本站会优先为端到端自动驾驶、BEV感知、3D目标检测、轨迹预测、路径规划、LiDAR感知等高价值论文补充中文说明。
Original abstract
Background and Rationale Sex differences in cancer incidence, progression, and mortality are well documented across multiple cancer types, yet the molecular mechanisms driving these disparities remain incompletely characterised. A central but underexplored question is whether the Warburg effect the metabolic hallmark of cancer involving preferential aerobic glycolysis, operates differently in male and female tumours, and if so, why. Objective This narrative review examines the molecular basis of sexual dimorphism in the Warburg effect across multiple cancer types, integrating evidence from sex hormone signalling, sex chromosome-linked gene regulation, epigenetic mechanisms, and interactions with the tumour microenvironment. Key Findings Four interconnected biological layers underlie sex-biased cancer metabolism. First, androgen receptor signalling functions as a near-universal pro-glycolytic driver in male-predominant cancers — directly transactivating GLUT1, HK2, and LDHA while estrogen receptor signalling exerts a more context-dependent, dual regulatory role, alternating between glycolytic promotion and oxidative redirection depending on glucose availability. Second, sex chromosome gene dosage establishes a hardwired metabolic asymmetry: females benefit from biallelic expression of the X-linked tumour suppressor KDM6A, which acts as an epigenetic brake on glycolytic chromatin remodelling, while males carry Y-linked genes such as KDM5D that promote immune evasion and metastasis, compounded by the metabolic instability caused by age-associated loss of the Y chromosome. Third, sex-biased epigenetic regulation, operating through histone modifications, X-inactivation escape, and metabolitedriven chromatin feedback, directly controls glycolytic gene accessibility in a sex-dependent manner. Fourth, the tumour microenvironment reflects and amplifies these differences through sex-specific patterns of immune cell metabolism, cancer-associated fibroblast behaviour, and adipose tissue distribution. Cancer-type analyses across breast, prostate, bladder, glioma, hepatocellular carcinoma, colorectal, and lung cancers confirm that these mechanisms are tissue-specific and cannot be reduced to a single male-biased rule. Conclusions and Implications Sex is a fundamental determinant of the Warburg effect at every level of biological organisation. Incorporating sexual dimorphism into metabolic cancer research from preclinical modelling to biomarker development and clinical trial design is essential for advancing precision oncology. Therapeutic strategies targeting aerobic glycolysis must account for the distinct hormonal, chromosomal, and epigenetic contexts that govern metabolic reprogramming in male and female tumors.
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