4.7 Article

Relationship between VEGF Family Members, Their Receptors and Cell Death in the Neoplastic Transformation of Colorectal Cancer

Journal

Publisher

MDPI
DOI: 10.3390/ijms23063375

Keywords

CRC; VEGF; apoptosis; diagnosis; tumor markers; gastrointestinal tract tumors; angiogenesis

Funding

  1. Medical University of Bialystok, Poland [SUB/1/DN/22/006/1198]

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Colorectal cancer is the second most common cause of cancer death globally. Both genetic and protein factors are involved in its pathogenesis. Researchers are exploring new diagnostic tools and potential therapeutic drugs, particularly VEGF family members related to blood vessel formation, which play a crucial role in colorectal cancer.
Colorectal cancer (CRC) is the second most common cause of cancer death in the world. Both modifiable and nonmodifiable risk factors play a significant role in the pathogenesis of this tumor. The diagnosis is usually made late due to limitations of screening tests; therefore, the scientists are looking for new diagnostic tools such as gene or miRNA expression or different proteins' concentrations, e.g., vascular endothelial growth factor (VEGF) family members. The VEGF family (VEGF-A, VEGF-B, VEGF-C, VEGF-D and PlGF) plays a key role in the processes of blood vessel formation in embryonic development as well as in pathological angiogenesis and lymphangiogenesis, which allow the tumor to grow exponentially. Blockage of VEGF-related pathways seems to be a valid therapeutic target. It was suggested in recent studies, that besides already used drugs, e.g., bevacizumab, there are other agents with potential usefulness in anticancer activity such as miRNAs, TMEA, granzyme K, baicalein and arginine. Moreover, VEGF proteins were assessed to induce the expression of anti-apoptotic proteins such as BCL-2 and BAX. Therefore, investigations concerning the usefulness of VEGF family members, not only in the development but also in the therapy of CRC, in order to fully elucidate their role in carcinogenesis, are extremely important.

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