MIR615 (MicroRNA 615)

Circulating miRNAs are valuable biomarkers for TKI resistance in CML. Targeting HMGB1-associated miRNAs, together with combined CBD and IM treatment, may help re-establish apoptotic regulation and overcome resistance mechanisms.

The Editor sincerely apologizes to the readership for any incovenience caused, and we thank the reader for bringing this matter to our attention. [Oncology Reports 39: 255‑263, 2018; DOI: 10.3892/or.2017.6079].

This study identifies circCNN2 as a novel oncogenic driver in endometrial cancer, operating through an m6A-regulated circRNA-miRNA-mRNA axis. The circCNN2/miR-615-5p/MYH14 pathway represents a promising therapeutic target for endometrial cancer treatment, particularly for patients with limited conventional therapy options. Our findings advance understanding of epitranscriptomic regulation in circular RNA biology and provide potential biomarkers for diagnosis and prognosis.

Knockdown of LRP11-AS1 inhibited in vivo growth of PTC tumor in nude mice model. LRP11-AS1 exhibited potential oncogenic effects in PTC by regulating the miR-615-3p/AKT2 axis, suggesting that LRP11-AS1 could serve as a potential diagnostic biomarker and therapeutic target in PTC.

The circKLHL24/Sec31A/miR-615-5p/CXCL12 axis is critical for CAF-induced PNI in PDAC. Therefore, circKLHL24 could serve as a potential therapeutic target for PDAC.

Downregulation of miR-615-5p was a prognostic indicator of poor prognosis in CC. miR-615-5p exerted its tumor-suppressive effects by inhibiting cell growth and metastasis through the regulation of TMIGD2.

This study reveals that vimentin affects the miR-615-3p-PICK1 axis through APA, revealing the key role of VIM in cancer progression. Opened up new avenues for targeted cancer therapy, with a focus on regulating the interaction between APA and miR-615-3p-PICK1.

Our results revealed that miR-615-3p modulated mTOR signaling, thus influencing the progression of OS. For OS treatment, molecular strategies that target the miR-615-3p/SESN2/mTOR pathway is promising.

RRFERV serves as an independent prognostic factor in NPC. During the malignant progression of NPC caused by high expression of RRFERV, ferroptosis can be induced to effectively kill cancer cells and reverse the radiotherapy resistance of NPC cells, suggesting a potential treatment approach for recurrent and refractory NPC.

It is likely that there are more miRs that regulate apoB-containing lipoprotein assembly and secretion. Discovery of additional miRs may uncover novel mechanisms that control lipoprotein assembly and secretion.

Furthermore, in vivo, animal experiments confirmed that circ-CDK8 interference inhibited OSCC cell proliferation and SLC7A11 expression. Collectively, this study revealed a novel strategy to upregulate erastin-induced ferroptosis in OSCC cells via the circ-CDK8/miR-615-5p/SLC7A11 axis, providing new insights into OSCC and a potential therapeutic strategy for OSCC.

The stability of circ_0023179 was verified using ribonuclease R enzyme, actinomycin D and agarose gel electrophoresis...The downregulation of miR-615-5p and the upregulation of CDH3 mitigated the inhibitory effect of silencing circ_0023179 on NSCLC cell proliferation. In conclusion, silencing circ_0023179 inhibited NSCLC cell proliferation by targeting the miR-615-5p/CDH3 axis involved in NSCLC progression.