Emerging role of exosome-derived non-coding RNAs in tumor-associated angiogenesis of tumor microenvironment

Abstract

The tumor microenvironment (TME) is an intricate ecosystem that is actively involved in various stages of cancer occurrence and development. Some characteristics of tumor biological behavior, such as proliferation, migration, invasion, inhibition of apoptosis, immune escape, angiogenesis, and metabolic reprogramming, are affected by TME. Studies have shown that non-coding RNAs, especially long-chain non-coding RNAs and microRNAs in cancer-derived exosomes, facilitate intercellular communication as a mechanism for regulating angiogenesis. They stimulate tumor growth, as well as angiogenesis, metastasis, and reprogramming of the TME. Exploring the relationship between exogenous non-coding RNAs and tumor-associated endothelial cells, as well as their role in angiogenesis, clinicians will gain new insights into treatment as a result.

Function and mechanism of exosomes derived from different cells as communication mediators in colorectal cancer metastasis

“…Exosomes derived from CRC encompass a diverse array of bioactive molecules that intricately modulate angiogenic processes and permeability alterations, thereby potentiating the invasive and metastatic potential of cancer cells. 73 Hu et al. discovered a significant elevation in miR-1229 levels within serum exosomes derived from CRC patients, which exhibited a strong correlation with tumor size, lymph node metastasis, TNM stage, and unfavorable prognosis.…”

Exosomal lncRNA SNHG12 promotes angiogenesis and breast cancer progression

“…Exosomes are naturally found in bodily fluids, such as blood, saliva, urine, and breast milk [ 11 ], making them potential biomarkers for the early detection of a variety of diseases [ 12 ]. Exosomal lncRNA has been reported to participate in tumor development, including growth, metastasis, and angiogenesis [ 13 ]. For example, ovarian cancer cell-derived exosomal lncRNA ATB promoted ovarian cancer growth and angiogenesis via the miR-204-3p/TGFβR2 axis [ 14 ].…”