The Role of Adipokines in Tumor Progression and Its Association with Obesity

The Role of Adipokines in Tumor Progression and Its Association with Obesity

3 January 2024 | Jae Won Kim, Jun Hyeok Kim, Yoon Jae Lee
Adipokines, bioactive molecules secreted by adipose tissue, play a critical role in linking obesity to tumorigenesis. Obesity is a major risk factor for various cancers, and adipokines such as leptin, adiponectin, visfatin, resistin, apelin, and chemerin contribute to the development and progression of tumors. Leptin promotes tumor growth, angiogenesis, and metastasis, while adiponectin exhibits tumor-suppressive effects by inducing apoptosis and cell cycle arrest. Visfatin and resistin also have pro-tumorigenic effects. Adipokines influence the tumor microenvironment by promoting inflammation, altering ECM composition, and modulating immune cell activity. They also affect cancer cell metabolism, including the Warburg effect, which supports tumor growth and metastasis. Adipokines can influence tumor progression through various signaling pathways, such as PI3K/Akt, MAPK, and STAT. Adiponectin, in contrast, has anti-tumor properties and is inversely associated with obesity-related cancers. The complex interplay between adipokines, tumor cells, and the tumor microenvironment highlights the potential of targeting adipokine signaling as a therapeutic strategy for obesity-associated cancers. Understanding the mechanisms by which adipokines influence tumorigenesis is crucial for developing novel cancer prevention and treatment approaches.Adipokines, bioactive molecules secreted by adipose tissue, play a critical role in linking obesity to tumorigenesis. Obesity is a major risk factor for various cancers, and adipokines such as leptin, adiponectin, visfatin, resistin, apelin, and chemerin contribute to the development and progression of tumors. Leptin promotes tumor growth, angiogenesis, and metastasis, while adiponectin exhibits tumor-suppressive effects by inducing apoptosis and cell cycle arrest. Visfatin and resistin also have pro-tumorigenic effects. Adipokines influence the tumor microenvironment by promoting inflammation, altering ECM composition, and modulating immune cell activity. They also affect cancer cell metabolism, including the Warburg effect, which supports tumor growth and metastasis. Adipokines can influence tumor progression through various signaling pathways, such as PI3K/Akt, MAPK, and STAT. Adiponectin, in contrast, has anti-tumor properties and is inversely associated with obesity-related cancers. The complex interplay between adipokines, tumor cells, and the tumor microenvironment highlights the potential of targeting adipokine signaling as a therapeutic strategy for obesity-associated cancers. Understanding the mechanisms by which adipokines influence tumorigenesis is crucial for developing novel cancer prevention and treatment approaches.
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