TL;DR
Functional rescue assays confirmed that miR‑17-5p mimic reversed the tumor‑suppressive effects of TRHDE‑AS1 overexpression, while PIK3R1 overexpression restored these inhibitory effects.
The ZNF582-AS1/miR-21-5p/miR-516a-3p/CREBRF regulatory axis provides mechanistic insights into EC tumorigenesis and emphasizes the tumor suppressive effect of ZNF582-AS1.
It is indicated that SLC12A9-AS1 is abnormally overexpressed in CRC cells and that its knockdown attenuates malignant phenotypes, at least in part through regulation of miR-139-3p.
RASAL2-AS1 exerts a tumor-suppressive effect in cervical cancer by functioning as a competing endogenous RNA (ceRNA) that modulates the miR-590-5p/PDCD5 axis and regulates the Wnt/β-catenin pathway.
Findings suggest that c-Myc-regulated AFAP1-AS1 may contribute to OSCC proliferation through modulation of the miR-655-3p/CCNA2 axis and provide insight into the molecular mechanisms underlying OSCC progression.
MNX1-AS1 promotes the progression of NSCLC by modulating the miR-218-5p/COMMD8 axis and acted as a molecular sponge for miR-218-5p, thereby relieving miR-218-5p-mediated repression of its direct target COMMD8.
It is suggested that lnc-DNAJC3-AS1 promotes GC progression, at least in part, through the miR-576-5p/LYPLA1 pathway, providing a potential target for GC treatment.
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