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The following is a summary of “MiR-4298 and lncKRTAP5-6-3 regulated Cathepsin D expression through ERK-MAPK signaling pathway in chronic UVB-damaged HaCaT cells,” published in the January 2025 issue of Dermatology by Chen et al. 

Researchers conducted a retrospective study to investigate the expression changes and interactions between miR4298 and lncKRTAP5-6-3 in UVB-damaged HaCaT cells and explore the role in the miR4298-MAPK/ERK signaling pathway-Cathepsin D-lncKRTAP5-6-3 mechanisms in photoaging.  

They irradiated HaCaT cells with 12 mJ/cm² UVB daily for 7 days, miR-4298 mimics and inhibitors were transfected using a lipo3000 transfection reagent. The HaCaT cells were categorized into 3 groups: blank control, UVB-damaged, and UVB-damage+miR-4298 regulation (overexpression or inhibition). The miR4298 and lncKRTAP5-6-3 expression levels were measured using RT-PCR, and Cathepsin D and MAPK/ERK pathway proteins were analyzed by Western blot.  

The results showed that after 7 days of UVB irradiation, miR-4298 expression decreased by 0.64 ± 0.06 (P < 0.001), and KRTAP5-6-3 expression dropped by 0.80 ± 0.13 (P < 0.001) compared to un-irradiated HaCaT cells, p-ERK signaling increased by 0.9437 ± 0.1186 (P < 0.0001), while Cathepsin D expression decreased by 0.6163 ± 0.075 (P < 0.0001). In miR-4298 mimic-transfected cells, lncKRTAP5-6-3 expression increased by 0.5114 ± 0.1438 (P < 0.05), p-ERK signaling decreased by 0.3880 ± 0.1185 (P < 0.01), and Cathepsin D expression increased by 0.2617 ± 0.0749 (P < 0.0001) compared to the UVB-damaged group. In miR-4298 inhibitor-transfected cells, lncKRTAP5-6-3 decreased by 0.1697 ± 0.1383, p-ERK signaling increased by 1.096 ± 0.7836 (P < 0.05), and Cathepsin D expression decreased by 0.05197 ± 0.24827 compared to the UVB-damaged group.  

Investigators concluded the synergistic effects of miR-4298 and lncKRTAP5-6-3 played key roles in chronic UVB-damaged HaCaT cells by regulating the MAPK/ERK signaling pathway and Cathepsin D expression, offering novel targets for addressing chronic ultraviolet damage (photoaging) and UV-related dermatoses. 

Source: frontiersin.org/journals/medicine/articles/10.3389/fmed.2024.1485224/full