MIR526B (MicroRNA 526b)

While ATP5A1 shows promise in tissue, plasma-based screening benefits from combining multiple markers, including pri-miR-526b. Further research is needed to refine plasma biomarker panels for effective early detection of breast cancer.

Its overexpression inhibited cancer cell proliferation, migration, and invasion while reducing tumor growth in xenografts. Oe-circITFG2 competitively bound miR-526b-5p, upregulating ITM2A to activate autophagy-mediated PD-L1 degradation and enhance antitumor immunity.

Overexpression of miR-526b and miR-655 may alter doxorubicin efficacy through mechanisms like DNA damage response changes, metabolic reprogramming, and immune pathway activation. Further investigation may uncover new therapeutic strategies to improve treatment efficacy and patient outcomes.

RNA-sequencing and network analyses identified hub genes involved in redox balance, immune, and metabolic pathways, which may have clinical significance (OAS2, TNF, CACNA1C, CALML5). Overall, these findings suggest that miR-526b, miR-655, and COX-2 play novel roles in promoting resistance to oxidative stress through transcriptional reprogramming in breast cancer; the identified markers could serve as potential biomarkers or therapeutic targets.

These findings indicate that a panel comprising miR-99a-5p, miR-516a-5p, and miR-526b-5p, alone or with established tumor markers, offers high accuracy as a minimally invasive diagnostic tool for CCA, and can effectively distinguish it from HCC.

HCP5 acts as an oncogenic lncRNA in GC by promoting cell viability, migration, and proliferation via the miR-526b/PBX3 axis. Targeting the HCP5/miR-526b/PBX3 axis may represent a promising therapeutic strategy for GC.

Mechanistically, circ-0003746 promotes epithelial-mesenchymal transition (EMT) by sequestering miR-526b, thereby advancing BCa progression. These findings highlight the role of circ-0003746 in regulating the miR-526b/EMT axis, positioning it as a potential biomarker for BCa.

Their ability to modulate multiple onco-genic and tumour-suppressive pathways highlights their potential as therapeutic targets or bi-omarkers in the context of personalized cancer treatment strategies. This review provides a com-prehensive depth of current knowledge while proposing avenues for future research into the ther-apeutic manipulation of these miRNAs in combating cancer.

Hesperetin exerted an interventional effect on the gastric carcinogenesis process, particularly through the modulation of exosomal circ0008274 and its interaction with miR-526b-5p.

miR-526b enhances inherent metabolic characteristics of breast cancer cell lines, increasing ATP production, proliferation, and resistance to metabolic inhibitors. Targeting the COX-2/EP4 axis mitigated some of the effects induced by miR-526b, but it did not normalize cell behavior, highlights the complex regulation of glucose metabolism in breast cancer and underscores the need for combination therapy strategies.

Overexpression of TP53 diminished the promotive effect of hsa-miR-526b-5p on ferroptosis-related proteins GPX4 and SLC7A11, whereas inhibition of TP53 reversed the impact of hsa-miR-526b-5p silencing. Our study demonstrates that hsa-miR-526b-5p targets TP53 to regulate 5-FU sensitivity in CRC through the ferroptosis pathway based on CRC organoid models.

Our study reveals that circPSD3 is a key regulator promoting PTC progression via the circPSD3/miR-526b/RAP2A pathway. Furthermore, we found that overexpressing BRAF, which inhibits circPSD3, significantly hampers the progression of PTC.