Molecular Mechanisms and Therapeutic Potential of Resolvins in Cancer-Current Status and Perspectives Publisher Pubmed

Summary: Research suggests resolvins from omega-3s may reduce cancer-related inflammation and tumor growth by clearing cell debris. #CancerResearch #Inflammation

Tajbakhsh A¹ ; Yousefi F² ; Farahani N³ ; Savardashtaki A^{1, 4} ; Reiner Z^{5, 6} ; Jamialahmadi T⁷ ; Sahebkar A^{7, 8}
Source: Current Medicinal Chemistry Published:2024

Abstract

Resolvins are specialized pro-resolving mediators derived from omega-3 fatty acids that can suppress several cancer-related molecular pathways, including important activation of transcription parameters in the tumor cells and their microenvironment, inflammatory cell infiltration, cytokines as well as chemokines. Recently, an association between resolvins and an important anti-inflammatory process in apoptotic tumor cell clearance (efferocytosis) was shown. The inflammation status or the oncogene activation in-creases the risk of cancer development via triggering the transcriptional agents, including nuclear factor kappa-light-chain-enhancer of activated B cells by generating the pro-in-flammatory lipid molecules and infiltrating the tumor cells along with the high level of pro-inflammatory signaling. These events can cause an inflammatory microenvironment. Resolvins might decrease the leukocyte influx into the inflamed tissues. It is widely ac-cepted that resolvins prohibit the development of debris-triggered cancer via increasing the clearance of debris, especially by macrophage phagocytosis in tumors without any side effects. Resolvins D2, D1, and E1 might suppress tumor-growing inflammation by activation of macrophages clearance of cell debris in the tumor. Resolvin D5 can assist patients with pain during treatment. However, the effects of resolvins as anti-inflammato-ry mediators in cancers are not completely explained. Thus, based on the most recent studies, we tried to summarize the most recent knowledge on resolvins in cancers. © 2024 Bentham Science Publishers.