MIR1304 (MicroRNA 1304)

This study demonstrates that TMIGD2 is downregulated in BLCA and correlates with adverse prognosis and immune regulation. Its potential as a prognostic biomarker and therapeutic target is underscored by its involvement in key pathways, immune infiltration, and drug sensitivity. Further research is essential to fully realize the clinical potential of TMIGD2 in the management of BLCA.

The miRNA-mRNA interactions were validated using real-time PCR in independent patient cohorts. This study revealed a complex molecular landscape of mCLM within the hepatic microenvironment and novel miRNA-mRNA interactions with potential prognostic and therapeutic implications.

A-to-I RNA editing alters the function of miR-1304-3p in ESCC by changing its target gene. The edited miR-1304-3p hinders the development of ESCC by inhibiting glycolysis and inactivating the Wnt5a/ROR2 signaling pathway.

This review consolidates current knowledge on the crosstalk between tumor cells and adipose tissue mediated by EVs and offers valuable insights for future research. It also addresses controversial topics in the field and possible therapeutic approaches to manage cancer cachexia and ultimately improve patient outcomes and quality of life.

Collectively, CAT2064 and CAT2042 and their miRNA targets may constitute a regulatory network in PCa, and could serve as novel biomarkers. The online version contains supplementary material available at 10.1007/s12291-021-00999-6.

It follows that the farnesyltransferase inhibitor (FTI) lonafarnib in addition to ALK TKIs act synergistically in neuroblastoma, inducing apoptosis in vitro. In particular, on combined treatment of neuroblastoma patient derived xenografts with an FTI and an ALK TKI complete regression of tumour growth is observed although tumours rapidly regrow on cessation of therapy. Overall, our data suggests that combined use of ALK TKIs and FTIs, constitutes a therapeutic approach to treat high risk neuroblastoma although prolonged therapy is likely required to prevent relapse.

Moreover, KLK11 was able to limit in vivo GC cell proliferation. These findings reveal a promising strategy to prevent and treat GC by targeting the KLK11-mediated mTOR/4E-BP1 cascade.

The inhibitory effects of circ_0060937 absence on A549 and H1299 cell malignant behaviors were largely reversed by miR-1304-5p inhibition or LAD1 overexpression, hinting that circ_0060937 affected lung cancer progression via modulating the miR-1304-5p/LAD1 axis. Circ_0060937 downregulation decreased the expression of LAD1 by releasing miR-1304-5p to effectively repress lung cancer cell growth and in vivo tumorigenesis.

Notably, a single nucleotide polymorphism (SNP) located in the miR-1304 stem-loop region shows a significant difference in frequencies of the G allele between African and Caucasian American groups, which promotes the maturation of miR-1304-3p. Therefore, our results reveal a mechanism of the disparity in breast cancer progression and suggest a potential utility of miR-1304-3p and the associated SNP as biomarkers for predicting the outcome of African American patients.

The circ_0068252/miR-1304-5p/PD-L1 signal axis participates in the regulation of DDP resistance and immune escape of NSCLC cells. Our results suggest that circ_0068252 may be a potential diagnostic marker and therapeutic target for DDP-resistant NSCLC.

Lastly, the functionalities of target genes were also revealed. The silencing characteristic of miRNAs might be exploited to design miRNA-mediated therapy that might potentially repress the overexpressed genes in carcinoma.

In this study, a different microRNA genes methylation landscape was shown in pediatric BCP ALL compared to children without neoplasms. A visible subcluster among BCP ALL samples consisted of individuals with TCF3-PBX1 genetic subtype. No other differences were observed in association with age, gender or risk group. Several interesting leukemia-connected phenotypes were found, associated with genes with hyperand hypomethylated sites located on promoters as well as gene bodies.