# Crosstalk Between Leptin and Adiponectin in Colorectal Cancer: Molecular Mechanisms and Oncogenic Pathways

## TL;DR

This paper explores how leptin and adiponectin influence colorectal cancer through different molecular pathways, offering insights into their opposing roles in cancer development.

## Contribution

The study provides a comprehensive overview of leptin and adiponectin signaling in colorectal cancer, emphasizing their contrasting effects on tumorigenesis.

## Key findings

- Leptin promotes CRC via JAK2/STAT3 and PI3K/Akt/mTOR pathways.
- Adiponectin inhibits CRC through AMPK and PPARα activation.
- The crosstalk between these adipokines is critical in CRC progression.

## Abstract

Colorectal cancer (CRC) remains one of the most common malignancies worldwide with relatively high levels of morbidity and mortality. Current data demonstrate the significant role of adipokines, in particular leptin and adiponectin, in CRC pathogenesis and progression. Both adipokines exert pleiotropic activities and often possess opposing physiological effects. The main goal of this study was to provide a comprehensive overview of current knowledge regarding the complex relationship between leptin and adiponectin signaling and tumorigenesis with a specific focus on CRC. The pro-tumorigenic role of leptin in CRC has been highly emphasized by recent reports, primarily by activation of JAK2/STAT3 and PI3K/Akt/mTOR signaling pathways. In contrast, adiponectin has been shown to demonstrate an anti-tumorigenic role mainly because of activation of AMPK and PPARα signaling cascades. Focusing on the current advances in the field of adipokines’ signaling, we highlighted the latest achievements in understanding their role in colorectal malignancy.