MIR1205 (MicroRNA 1205)

We also high-light emerging evidence on exosomal circRNAs like circ_0006174, linked to doxorubicin re-sistance through miR-1205/CCND2 axis modulation. These exo-ncRNAs have shown promise as biomarkers and potential therapeutic targets, with studies indicating their diagnostic and prog-nostic capabilities in CRC patient cohorts. By examining recent in vivo and in vitro studies, we offer a comprehensive understanding of exosomal ncRNAs' roles in CRC pathogenesis and po-tential applications in clinical trials.

Moreover, the loss of donor and acceptor splice site was evident. Our results highlight the importance of non-coding regions that might boost our research capacity to predict and construct targeted therapeutic approaches.

The effect of circSLC4A7 on DR was also confirmed by xenograft experiments. Collectively, circSLC4A7 in resistant-cells-derived exosomes promotes DCT resistance of PCa via miR-1205/MAPT axis, which may provide a new treatment strategy for DR of PCa.

Complex network analysis highlighted both extracellular matrix and cardiovascular remodelling (since visit 1) as well as inflammation (at visit 4) as key features of early GFR decrease. These findings lay the foundation to further assess whether the proteins and genes herein identified may represent potential biomarkers or therapeutic targets to prevent renal function impairment.

This study demonstrated the pro-metastatic role of miR-1205 in breast cancer, mediated via a novel miR-1205/CDK3/Snail axis. Moreover, we identified miR-1205 and CDK3 as potential markers of invasion and progression in breast cancer.

Mechanistically, our results indicated that circMYBL2 promoted E2F1 expression and facilitated HCC progression by sponging miR-1205. Our findings revealed that circMYBL2 contributed to HCC progression through the circMYBL2/miR-1205/E2F1 axis, suggesting the potential of circMYBL2 as a novel target for HCC treatment or a prognostic biomarker for HCC.

In summary, our study demonstrated that circIL21R was highly expressed in cervical cancer and upregulated PTBP1 expression by acting as a ceRNA for miR-1205, making outstanding contributions to several malignant biological processes in cervical cancers, such as growth, proliferation, and invasion. CircIL21R is a potential biomarker for the diagnosis and treatment of cervical cancer.

Furthermore, LINC00900 promoted GSC viability, invasion, self‑renewal and tumor growth by regulating the miR‑1205/STAT3 axis. In conclusion, YTHDF1 promotes GSC viability and self‑renewal by regulating the LINC00900/miR‑1205/STAT3 axis.

Importantly, circARFGEF2 silencing significantly inhibited LN metastasis in the KrasG12D/+Trp53R172H/+Pdx-1-Cre (KPC) mouse PDAC model. These findings provide insight into the mechanism and metastasis-promoting function of mutant KRAS-mediated circRNA biogenesis.

Mechanistically, circMYBL2 upregulated the transcription factor E2F1 by sponging miR-1205 and complexing with eukaryotic translation initiation factor 4A3 (eIF4A3) and then facilitated the epithelial-mesenchymal transition (EMT) process in BC cells. Our findings showed that circMYBL2 promoted the tumorigenesis and aggressiveness of BC through the circMYBL2/miR-1205/E2F1 and circMYBL2/eIF4A3/E2F1 axes, which may provide a novel targeted therapy for patients with BCLM.

Circ_0137652 controls the miR-1205/CCNB1 axis to induce increased breast cancer malignancy. Our findings suggest that circ_0137652 may be a novel target for BC therapy.

Mechanistically, miR-1205 suppresses HCC cell proliferation via a CSNK2B/CDK4 axis. The present results indicated that miR-1205 suppressed HCC cell proliferation by directly targeting CSNK2B and thus inhibiting the CDK4/pRb cell cycle pathway.