MIR338 (MicroRNA 338)

This study implies that the resistance of SMMC-7721/OXA cells to OXA is likely related to the acquisition of the EMT phenotype. The up-regulating miR-338-3p could be a new treatment method for over-coming OXA resistance in hepatocellular carcinoma.

Further investigation demonstrated that miR-338-3p exerts its tumour-suppressive effects by directly targeting ETS1, and the hsa_circ_0000977/miR-338-3p/ETS1 axis regulates the proliferation and migration of CCA cells. We have concluded that hsa_circ_0000977 drives CCA progression by sponging miR-338-3p and modulating its target ETS1, suggesting its clinical value for predicting outcomes and developing targeted therapies.

miR-338-3p directly targets WAPL to downregulate its expression, thereby suppressing the proliferative and invasive capacities of cervical cancer cells. These findings provide mechanistic insights into the post-transcriptional regulation of WAPL in cervical cancer.

Therefore, the article must be retracted. The authors did not respond to communications from the Publisher regarding the retraction.

Knockdown of circPSD3 disrupts the TCA cycle and impairs mitochondrial function, resulting in decreased membrane potential and aerobic respiration rate. The reduction in mitochondrial function resulted in the inhibition of proliferation and initiation of mitochondria-mediated apoptosis.

However, whether cancer-secreted sEVs affect the progression of doxorubicin-induced cardiotoxicity (DOXIC) via orchestrating the tumor cell-cardiomyocyte crosstalk has not yet been explored...Our findings uncovered for the first time that DOX-treated BCCs exacerbated DOXIC through releasing pro-ferroptotic miR-338-3p-enriched sEVs. Therefore, targeting sEVs-mediated tumor/cardiomyocyte pathological communication may offer a novel approach for the management of DOXIC.

This work establishes a versatile CRISPR-microfluidic platform for cancer diagnosis. Its modular design allows for adaptation to detect other cancer-related RNA biomarkers, thereby addressing critical needs in precision oncology.

Furthermore, treatment with miR-219/miR-338 significantly improved sensory and locomotor recovery of injured mice starting 4 weeks post-treatment, and kinematic analysis further demonstrated enhanced motor coordination and gait patterns. Collectively, these findings suggest that enhanced OL remyelination improves functional recovery even in a more challenging complete transection SCI paradigm when mice were treated with fiber-hydrogel scaffolds loaded with miR-219/miR-338.

Exosome-mediated delivery of miR-338-3p offers a promising approach for gastric cancer therapy by reducing tumor adhesion to mesothelial cells. This strategy underscores the potential of exosome-based miRNA therapies for the treatment of advanced gastric cancer.

Based on the obtained data, circ_PSD3 promotes PTC cell proliferation, migration, invasion and EMT by regulating the miR-145-5p/miR-338-3p/HMGB3 axis. The current work revealed the mechanism of action of circ_PSD3 in PTC and may play the role of a new medical target for PTC.

Furthermore, by decreasing the miR-338-3p overexpression sensitivity to Lenvatinib-induced cell death in HCC cells, SOX4 may be a potential therapeutic candidate. In conclusion, miR-338-3p has a considerable function in liver CSC self-renewal and tumor development, making it a promising therapeutic target against HCC.

Notably, the CMD panel showed exceptional potential for distinguishing early-stage OC samples from healthy controls, achieving an AUC of 1. In this study, we elucidated the functional mechanisms of a set of circRNAs associated with OC through multi-omics analysis and demonstrated that the combination of circRNAs and miRNAs into a biomarker panel holds significant potential for early detection of ovarian cancer.