MIR3163 (MicroRNA 3163)

Hsa_circ_0062522 affects the activity, migration, apoptosis and TAM resistance of ER + breast cancer cells in vitro through miR-3163. In vivo, it influences the volume, weight and TAM sensitivity of tumors.

This study unveils a novel regulatory pathway involving EXO1/Polη/Polι axis and miR-3163, providing insights into CSLCs regulation in NSCLC. EXO1/Polη/Polι axis targeted by miR-3163, resulting in the inhibition of cell growth and induction of apoptosis in NSCLC CSLCs.

Furthermore, we establish SOX-2 as a direct target of miR-3163 through dual-luciferase assay. Taken together, our study demonstrates that overexpression of miR-3163 could be a promising strategy for efficiently eradicating the CSC population to prevent chemoresistance and tumor relapse in ovarian cancer patients.

Finally, lncRNA CBR3-AS1 knockdown inhibited tumor growth and suppressed cancer stem cell-like properties of cervical cancer in vivo. Taken together, high expression of lncRNA CBR3-AS1 predicts poor prognosis in cervical cancer, and the lncRNA CBR3-AS1/miR-3163/LASP1 pathway plays a vital function in the modulation of cervical cancer cell proliferation and cancer stem cell-like properties.

Animal assay certified that FAM201A expedited CRC cell growth in vivo. In conclusion, our study was the first to unveil that FAM201A promoted cell proliferation and CSC characteristics in CRC via regulation of the miR-3163/MACC1 axis, which provided clues for the clinical treatment of patients with this disease.

Met exerts its antitumor activities by regulating the AFAP1-AS1/miR-3163/SPP1/PI3K/Akt/mTOR axis. Our findings deepen our understanding of mechanisms underlying anti-tumor effect of Met in LUAD.

Moreover, NF-κB signaling inhibition reversed the oncogenic effects of both SCIN and MEX3A. In summary, our results demonstrate that MEX3A may promote NPC development and progression via the miR-3163/SCIN axis by regulating NF-κB signaling, thus providing a potential target for NPC treatment.