Erythropoietin-induced hepatocyte receptor A2 regulates effect of pyroptosis on gastrointestinal colorectal cancer occurrence and metastasis resistance

Abstract

Erythropoietin-induced hepatocyte receptor A2 (EphA2) is a receptor tyrosine kinase that plays a key role in the development and progression of a variety of tumors. This article reviews the expression of EphA2 in gastrointestinal (GI) colorectal cancer (CRC) and its regulation of pyroptosis. Pyroptosis is a form of programmed cell death that plays an important role in tumor suppression. Studies have shown that EphA2 regulates pyrodeath through various signaling pathways, affecting the occurrence, development and metastasis of GI CRC. The overexpression of EphA2 is closely related to the aggressiveness and metastasis of GI CRC, and the inhibition of EphA2 can induce pyrodeath and improve the sensitivity of cancer cells to treatment. In addition, EphA2 regulates intercellular communication and the microenvironment through interactions with other cytokines and receptors, further influencing cancer progression. The role of EphA2 in GI CRC and its underlying mechanisms provide us with new perspectives and potential therapeutic targets, which have important implications for future cancer treatment.

Keywords: Colorectal cancer; Pyroptosis; Erythropoietin-induced hepatocyte receptor A2; Tumor metastasis; Drug resistance

Core Tip: This study investigated the expression of erythropoietin-induced hepatocyte receptor A2 (EphA2) in gastrointestinal (GI) colorectal cancer (CRC) and the mechanism by which EphA2 regulates pyroptosis. By reviewing the relevant literature, we found that EphA2 regulates pyroptosis through a variety of signaling pathways (such as the phosphatidylinositol 3 kinase/protein kinase B and Ras/mitogen-activated protein kinase pathways), thereby affecting the survival, proliferation and metastasis of cancer cells. The abnormal expression of EphA2 is closely related to the malignant behavior of GI CRC, and EphA2 further regulates the tumor microenvironment and immune response through interactions with inflammatory factors (such as tumor necrosis factor-α and interferon-γ). Studies have shown that targeting EphA2 can induce pyrodeath in cells, improve the sensitivity of cancer cells to treatment, and subsequently inhibit the occurrence and metastasis of tumors. Therefore, an in-depth understanding of the molecular mechanism by which EphA2 regulates pyrodeath provides new ideas and potential targets for the treatment of GI CRC.