MIR513A1 (MicroRNA 513a-1)

Collectively, this study identifies circBRWD1 as a key oncogenic circRNA that facilitates HBV replication and HCC progression via the miR-513a-5p/TNPO1 axis. Targeting circBRWD1 may offer a novel therapeutic strategy for HBV-related HCC, potentially addressing the challenge of HBV persistence and improving patient outcomes.

These findings identify circTTC13 as a critical driver of HCC progression and resistance to drug-induced ferroptosis via upregulation of SLC7A11. The cicTTC13/miR-513a-5p/SLC7A11 axis represents a potential therapeutic target for HCC.

In particular, we found that long non-coding RNA MIR4435-2HG acted as ceRNA sponging miR-513a-5p to promote the expression of BCL2L1, thereby promoting pancreatic cancer cells proliferation. In conclusion, BCL2L1 expression regulated by the MIR4435-2HG-miR-513a-5p-BCL2L1 ceRNA axis might be used as a biomarker for cancer prognosis, treatment selection, and follow-up in PAAD patients.

As a tumor suppressor, circEPHA3 inhibited the proliferation and metastasis of PCa cells through the miR-513a-3p/BMP2 axis, suggesting that circEPHA3 might be a potential therapeutic target for PCa.

Mechanistically, circHGS functions as a sponge of miR-513a-5p to elevate VEGFC expression and activate the AKT/mTOR signaling pathway, ultimately promoting BCa progression. Our findings indicated that circHGS promotes BCa progression via the miR-513a-5p/VEGFC/AKT/mTOR pathway and can be a promising therapeutic target of BCa.

Furthermore, circSEC61A1 could regulate PEX5 expression through competitive absorption of miR-513a-5p. Generally, circSEC61A1 is a potential biomarker for NSCLC, and circSEC61A1 serves tumor-promoting action in the progression of NSCLC.

In addition, as a key transcription factor of Warburg effect related genes, SIX1 was proved to enhance the transcriptional expression of LDHA by chromatin immunoprecipitation assay, thereby regulating glycolysis in colon cancer cells. Therefore, we identified that circPLOD2 promoted colon cancer progression through miR-513a-5p/SIX1/LDHA axis, and acted as a new biomarker for colon cancer prognosis and treatment.

The reduced LINC01234 exerts inhibitory impacts on pancreatic cancer cells via targeting miR-513a-3p to restrain H6PD level. The current study broadens the understanding of LINC01234 function and affords novel therapeutic targets for pancreatic cancer treatment.

5-FU sensitivity was enhanced after circ_0003998 level reduction in vivo. These findings unraveled that circ_0003998 elevated 5-FU resistance in HCC by sponging miR-513a-5p to upregulate the level of ARK5, indicating that circ_0003998 might be used as a target to improve 5-FU therapy for HCC.

In conclusion, downregulation of BBOX1-AS1 inhibits cell proliferation, and metastasis accelerates cell apoptosis and ferroptosis in ESCC by upregulating miR-513a-3p to reduce SLC7A11 expression. These findings may provide novel insights into the diagnosis and treatment of ESCC.

Based on our results, the transcriptome profile of ARDS patients would be a valuable source for understanding molecular mechanisms of host response and developing clinical guidance on anti-inflammatory medication.

The rescue experiment showed that cotransfection with circRNA.0007127 small-interfering RNA (siRNA) and the miR-513a-5p inhibitor increased CASP8 gene expression and the apoptosis rate, suggesting that the miR-513a-5p inhibitor is a circRNA.0007127 siRNA antagonist. CircRNA.0007127 regulates K-562 cell apoptosis through the miR-513a-5p/CASP8 axis, which can serve as a novel powerful molecular target for K-562 cells.