Harnessing tumorous flaws for immune supremacy: is miRNA-155 the weak link in breast cancer progression?

Abstract

With the advent of immune checkpoint blockade (ICB) therapy, treatment strategies for late-stage cancers have seen a radical advancement. In this issue of the JCI , Wang et al. characterize the functional role of miR-155 in breast cancer and its potential in harnessing the efficacy of immunotherapy. The study reports that high expression levels of miR-155 in breast cancer cells downregulated suppressor of cytokine signaling 1 (SOCS1), increased the phosphorylated STAT1 (pSTAT1)/pSTAT3 ratio, and thereby stimulated chemoattractants for tumor infiltration of effector T cells. Moreover, miR-155 overexpression set the stage for ICB therapy via increased programmed death ligand 1 (PD-L1) expression on cancer cells and enhanced immunological memory response via the release of miR-155–containing extracellular vesicles. Collectively, these data suggest that miR-155 is a strong candidate as a prognostic biomarker for ICB therapy.

Extracellular Vesicles and Their Zeta Potential as Future Markers Associated with Nutrition and Molecular Biomarkers in Breast Cancer

“…The underexpression of PTEN promotes the inhibition of Akt, a pathway that has already been reported to be deregulated in breast cancer [ 117 , 118 ]. Additionally, the expression of miRNA-155 has been previously reported and associated with resistance to antineoplastic treatment [ 36 , 119 , 120 ], tumor recurrence, and progression [ 119 , 121 , 122 ]. Likewise, the expression of miRNA-155 has been reported in EVs in diseases such as kidney cancer [ 123 ], lung injury [ 33 ], brain injury [ 124 ], and epilepsy [ 125 ], among others.…”

Mapping the function of MicroRNAs as a critical regulator of tumor-immune cell communication in breast cancer and potential treatment strategies

“…For example, in breast cancer cells, miR-34a replacement inhibited migration and proliferation, but in TNBC cells, miR-544 and miR-603 replacements reduced invasion and proliferation. Research into miRNA suppression has focused on oncomiRs such as miR-21 and miR-214 because of the promise they hold for preventing the advancement of cancer by modulating certain genes and signalling pathways ( Sharma S. et al, 2022 ).…”

Non-Coding RNAs as Potential Targets for Diagnosis and Treatment of Oral Lichen Planus: A Narrative Review

“…miR-155 is transcribed from the host gene MIRHG155, which is also known as the B cell integration cluster, located on chromosome 21 [79]. Pre-miR-155, a 65 nt long stem-loop precursor, is converted from pri-miR-155 in the nucleus and then further processed in the cytoplasm to create the miR-155 duplex, a 22-nucleotide structure with -5p and -3p strands.…”