C1q/TNF-related protein 6 (CTRP6) is emerging as a critical regulator of cancer biology with direct implications for clinical outcomes. Across a wide spectrum of malignancies, CTRP6 plays a central role in coordinating key oncogenic processes and linking metabolic, inflammatory, and signaling pathways that drive tumor progression. While CTRP6 generally promotes oncogenic behavior in cancers such as hepatocellular carcinoma, lung cancer, and clear cell renal cell carcinoma, conflicting findings have been reported in gastric cancer and oral or head and neck squamous cell carcinoma, where its tumor-promoting versus tumor-suppressive roles remain unresolved. CTRP6 has been shown to modulate fundamental processes including angiogenesis, ferroptosis, proliferation, apoptosis, migration, invasion, and inflammation. These effects are primarily mediated through activation of the PI3K/AKT and MEK/ERK signaling pathways, which are central to tumor growth, metastasis, and therapeutic resistance. Beyond its mechanistic roles, CTRP6 demonstrates potential as a diagnostic and prognostic biomarker, with altered expression patterns linked to cancer initiation, progression, and patient survival. Inhibition of CTRP6 in preclinical models enhances ferroptotic cell death and suppresses tumor progression, highlighting its promise as a therapeutic target. By consolidating current evidence from multiple cancer models, this review provides a comprehensive overview of CTRP6’s contributions to oncogenesis and underscores its dual potential as both a biomarker and a therapeutic target. Advancing a deeper understanding of CTRP6 in specific tumor contexts will be critical for unlocking its clinical utility and may open new opportunities to improve diagnosis, optimize therapeutic strategies, and ultimately enhance patient outcomes.
C1q/肿瘤坏死因子相关蛋白6（CTRP6）正逐渐成为癌症生物学中的关键调控因子，对临床结局具有直接影响。在多种恶性肿瘤中，CTRP6通过协调关键的致癌过程，并连接驱动肿瘤进展的代谢、炎症及信号通路，发挥着核心作用。尽管CTRP6通常在肝细胞癌、肺癌和透明细胞肾细胞癌等癌症中促进致癌行为，但在胃癌及口腔或头颈部鳞状细胞癌中的研究结果存在矛盾，其促癌与抑癌作用尚未明确。研究表明，CTRP6可调控血管生成、铁死亡、增殖、凋亡、迁移、侵袭及炎症等基本生物学过程。这些效应主要通过激活PI3K/AKT和MEK/ERK信号通路介导，而这些通路对肿瘤生长、转移及治疗抵抗至关重要。除机制性作用外，CTRP6还显示出作为诊断和预后生物标志物的潜力，其表达模式的变化与癌症发生、进展及患者生存密切相关。临床前模型中抑制CTRP6可增强铁死亡并抑制肿瘤进展，凸显了其作为治疗靶点的前景。本文通过整合多类癌症模型的现有证据，全面概述了CTRP6在肿瘤发生中的作用，并强调其作为生物标志物和治疗靶点的双重潜力。深化对CTRP6在特定肿瘤背景下作用的理解，对于开发其临床应用价值至关重要，并可能为改善诊断、优化治疗策略及最终提升患者预后开辟新途径。
CTRP6 in Cancer: Mechanistic Insights and Therapeutic Potential
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