MIR625 (MicroRNA 625)

Our study suggest that the manipulation of POC1B-AS1/miR-625-5p/FOXK1 pathway-mediated aggressiveness in CRC may offer an effective therapeutic target.

The inhibitory effects of LNC511 on LC were reversed by either overexpressing miR-625 or downregulating LOXL4, while a specific agonist of the Wnt/β-catenin pathway also negated these effects. In conclusion, LNC511 inhibits LC cell proliferation and stemness by sponging miR-625, promoting LOXL4 expression and consequently inactivating the Wnt/β-catenin signaling pathway.

Molecular dynamics simulations suggested potential direct interactions between PDGFB and osimertinib, providing additional insights into the resistance mechanism. Our study identifies a novel circROBO2/miR-625-5p/PDGFB regulatory axis in osimertinib resistance and positions circROBO2 as a potential therapeutic target and biomarker for NSCLC treatment.

Cell Counting Kit-8 (CCK-8) assay revealed that RIPOR1 promoted cell proliferation in CRC. RIPOR1 has a significant impact on the development and proliferation of CRC, and may be a potential predictive biomarker.

Inhibition of the lncRNA FTX/miR-625-5p/SLC7A11 axis can induce ferroptosis and disturb intracellular redox balance, further sensitizing CRC cells to ionizing radiation, suggesting its potential as a therapeutic target for improving CRC response to radiation therapy.

Although biomarker-driven therapies have improved treatment, responses to standard chemotherapeutics, such as 5-fluorouracil (5-FU), oxaliplatin, and irinotecan, vary considerably. Despite these promising findings, the clinical translation of miRNA-based biomarkers faces challenges, including methodological inconsistencies and the dynamic nature of miRNA expression, influenced by the tumor microenvironment. This review highlights the critical role of miRNAs in elucidating chemoresistance mechanisms and their promise as biomarkers and therapeutic targets in CRC, paving the way for a new era of precision oncology.

MiR-625 can be a promising approach to aid in the treatment of AML. However, further studies are required in this field.

circEEF2 activated the Hedgehog pathway through the miR-625-5p/TRPM2 axis, promotes mitochondrial stress, and promotes PCa development in vivo. circEEF2 upregulates mitochondrial stress to promote PCa by activating the Hedgehog pathway through the miR-625-5p/TRPM2 axis.

qRT-PCR indicated both IL32, VCAM1, and NFKB1 were potential markers under US-guided MWA-related time series analysis. The use of US-guided MWA might be a practical method for influencing the function of target genes, regulating time frames to decrease inflammation, and stimulating immune responses in glioma therapy.

In conclusion, the identification of specific miRNAs as predictors of TTFT holds promise for enhancing risk stratification in CLL to predict therapeutic needs. However, further validation studies and in-depth functional analyses are required to confirm the robustness of these observations and to facilitate their translation into meaningful clinical utility.

In vivo assays showed that HAGLR knockdown inhibited PC cell growth by regulating the TAF15 expression. These findings suggest HAGLR could facilitate PC cell malignant behaviors through regulating the TAF15 expression, demonstrating that HAGLR might be a valuable target for the PC treatment.

A regulatory network, including solasonine, miRNAs, and mRNAs related to BC, was constructed. This network provides extensive insights into the molecular regulatory mechanisms that underlie the anti-cancer efficacy of solasonine in BC.