MIR1293 (MicroRNA 1293)

This study is the first to demonstrate that hsa_circ_0007439 functions as a competitive endogenous RNA to upregulate KRT1 expression, thereby promoting the metastasis of NPC, suggesting that hsa_circ_0007439 serve as a potential diagnostic biomarker and therapeutic target for NPC.

Furthermore, a nomogram integrating the miRNA-based model with Milan criteria (MC) was developed and exhibited a high predictive accuracy (AUC =0.926, P<0.001) and clinical applicability, which was remarkably better than that of MC (AUC =0.629, P<0.001). This model may contribute to the reasonable selection of LT candidates in HCC patients and the personalized postoperative management.

The anti-miR-1293 group, in comparison to the anti-NC group, had slower tumor growth in mice, increased mRNA and protein expressions of PPARGC1A in tumor tissues, as well as reduced tumor volume and weight, expression of miR-1293 and degree of tumor malignancy. MiR-1293 facilitates oral carcinoma cell proliferation and metastasis by suppressing the expression of PPARGC1A.

In addition, miR-1293 promoted tumor growth in vivo. This study revealed the regulatory role of miR-1293 in HCC is related to the participation of METTL3-mediated m6A methylation, which could provide new therapeutic strategies for HCC.

Additionally, differential expression of miR-27a, miR-221, and miR-224 in treatment-sensitive versus treatment-resistant patients indicated their predictive biomarker potential for treatment response of cervical cancer patients. Conclusively, this study has identified 18 promising miRNAs for the development of sensitizers for thermoradiotherapy and may provide potential biomarkers for predicting treatment response in locally advanced cancers.

Subsequent rescue experiments revealed that TIMP1 overexpression reversed the impact of circSCAF8 shRNA viruses on gastric cancer. In conclusion, circSCAF8 expression was elevated in gastric cancer, and circSCAF8 shRNA viruses inhibited gastric cancer growth and metastasis by upregulating TIMP1 expression via miR-1293.

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.

We have identified core genes associated with non-small cell resistance to entrectinib, including CHI3L2, ZEB2, and S100A12. ZEB2 is a core gene associated with acquired resistance to entetinib in NSCLC.

Finally, with in vivo assay, we found obvious Spry4 up-regulation and VEGF-A, bFGF, ERK1/2 phosphorylation, micro-vessel density marker CD31 expression down-regulation in vivo, respectively. Collectively, these results indicated that miR-1293 knockdown could significantly attenuate LUAD angiogenesis via Spry4-mediated ERK1/2 signaling inhibition, which might be helpful for uncovering more functions of miR-1293 in LUAD and providing experimental basis for possible LUAD therapeutic strategy targeting miR-1293.

Our study offers a novel approach to constructing intercellular communication networks using snRNA-seq and exosome-small RNA sequencing. By integrating miRNA tracing with ligand-receptor analysis, we illuminate the complex interactions in the pancreatic cancer microenvironment, highlighting the pivotal role of miRNAs and identifying potential biomarkers and therapeutic targets.

Furthermore, miR-1293 inhibits osteosarcoma progression by targeting TIMP1 to inactivate the Notch1/Hes1 and TGFBR1/Smad2/3 pathways, thereby promoting tumour cell death. The findings presented herein unveil a novel mechanism for enhancing cisplatin sensitivity and proposed a potential therapeutic strategy for osteosarcoma through pre-chemotherapy supplementation of miR-1293.

Low expressions of CADM3-AS1, LINC00092, and ZNF667-AS1 in ceRNA network were probably promising poor prognostic biomarkers for CESC patients. The genes show a prospective research area for CESC-targeted treatment in the future.