CREG1 Human

CREG1 was first discovered due to its interaction with the adenovirus E1A oncoprotein. The E1A protein is known for its role in transforming cells and activating transcription. CREG1 counteracts these effects, thereby acting as a cellular repressor. This discovery highlighted the potential of CREG1 as a therapeutic target for diseases involving abnormal cell growth and transformation .

One of the critical functions of CREG1 is its involvement in vascular remodeling. Studies have shown that CREG1 is a lysosomal glycoprotein that helps maintain vascular homeostasis. It has been observed that CREG1 gene expression is significantly decreased in remodeled vascular tissues, particularly in response to angiotensin II (Ang II). This downregulation is specific to Ang II and independent of blood pressure . The reduction in CREG1 expression leads to vascular hypertrophy and fibrosis, which are characteristic features of hypertensive vascular remodeling .

CREG1 also exhibits tumor-suppressive properties. It has been shown to inhibit invasive cell growth and reduce the proliferation, migration, and invasion of tumor cells. This effect is particularly evident in the context of breast cancer, where CREG1 levels are negatively regulated by cathepsin B, a lysosomal protease. The overexpression of cathepsin B leads to a decrease in CREG1 levels, promoting tumor growth and invasion. Conversely, the inhibition or deletion of cathepsin B results in increased CREG1 levels, thereby suppressing tumor progression .

Given its role in vascular remodeling and tumor suppression, CREG1 holds significant therapeutic potential. It may serve as a target for interventions aimed at preventing hypertensive vascular diseases and certain types of cancer. The recombinant form of CREG1 has been studied for its protective effects against angiotensin II-induced hypertension and myocardial fibrosis, further underscoring its therapeutic relevance .