# CTRP6 in Cancer: Mechanistic Insights and Therapeutic Potential

## TL;DR

CTRP6 is a protein involved in cancer progression and treatment resistance, with potential as a diagnostic marker and therapeutic target.

## Contribution

This review consolidates current evidence on CTRP6's roles in cancer, highlighting its dual potential as a biomarker and therapeutic target.

## Key findings

- CTRP6 modulates cancer progression through pathways like PI3K/AKT and MEK/ERK.
- CTRP6 inhibition in preclinical models enhances ferroptotic cell death and suppresses tumor growth.
- CTRP6 expression patterns correlate with cancer initiation, progression, and patient survival.

## Abstract

C1q/TNF-related protein 6 (CTRP6) is a protein that plays important roles in how cancer develops and progresses. It can influence blood vessel formation, cell growth, cell survival, spread of cancer cells, and resistance to treatment. Recent studies also show that CTRP6 may help cancer cells escape a special type of cell death called ferroptosis, which has become an exciting target for new therapies. Because CTRP6 appears to work differently depending on the cancer type, it may serve as both a useful marker for disease and a potential treatment target. In this review, we bring together current knowledge about how CTRP6 affects cancer, highlight the key signaling pathways it controls, and discuss how targeting this protein could open new directions for therapy. Our goal is to provide a clear overview of CTRP6 in cancer to guide future research and therapeutic strategies.

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.