MIR33A (MicroRNA 33a)

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.

We also identified the tumor suppressor role of miR-17-5p, which was associated with higher Gleason scores. We propose PRC1, UBA52, RCC1, miR-124-3p and miR133a-3p as stage-specific PCa identifiers.

Specifically, we highlight the modulatory roles of miRNA in cancer cell survival and proliferation (miR-28, miR-30b/c), invasion and metastasis (miR-218, miR-182), neoangiogenesis (miR-29c), metabolic reprogramming (miR-124), and therapy resistance (miR-378, miR-328, miR-1244). The broad implications of miRNAs in lung cancer underline their potential real-world utility, as these entities can function as biomarkers for prognosis/diagnosis and even future therapeutic targets or agents.

The work aimed at exploring the potential mechanism of Long noncoding RNA tyrosine protein kinase transmembrane receptor 1 antisense RNA 1 (ROR1-AS1) in the process of epithelial-mesenchymal transition (EMT) of pancreatic cancer (PC) cells resistant to Gemcitabine (GEM)...ROR1-AS1 modulates the growth and EMT process of PC through the miR-33a-5p/HMGB1 axis. ROR1-AS1 knockdown or miR-33a-5p overexpression is effective to reduce GEM resistance in PC.

TIA1 gene, stress granule (SG) marker, is tightly regulated by miR-33a/KDM5C/H3K4me3 axis and exosomal miR-33a diminishes the formation of stromal SGs in CAFs. Collectively, our study reveals tumour selectively secretes miR-33a-5p through EVs to remodel the stromal SG formation and gain survival possibility for cancer cells in tumour core region, highlighting a novel regulatory mechanism of iron and nutrient level on EV secretion and the function of polyamine metabolism in reshaping epigenetic profiles.

By synthesizing current evidence, this review provides a consolidated resource to guide future mechanistic studies and therapeutic development. This review highlights promising molecular targets and emerging strategies to enhance radiosensitivity and offers a foundation for translational research aimed at improving outcomes in radiation-refractory breast cancer.

While not statistically significant, ROC curve of miR-133b suggests a potential role in predicting metastatic risk, warranting subsequent analysis. This study provides evidence for further evaluation of miR-221, miR-320a, miR-133a, and miR-133b as biomarkers in primary diagnosis and assessment of metastatic risk in leiomyosarcoma.

In aggregate, our findings unveil the circPVT1/miR-33a-5p/Myc/GLS1 axis as a pro-tumorigenic metabolic event sustaining breast cancer transformation with potential therapeutic implications.

The consistent findings across independent studies emphasize their potential clinical utility in early detection, prognostic assessment, and therapeutic targeting. However, further validation in larger and more diverse populations, along with the standardization of detection methods, is necessary before these biomarkers can be implemented in clinical practice.

The FBXL16 protein expression in Ishikawa/MPA-R cells was significantly higher compared with Ishikawa cells, and the mRNA and protein expression levels of FBXL16 were markedly elevated in the PPVII + miR-33a-5p inhibitor group compared with the PPVII + NC group (P<0.01). These findings suggested that PPVII upregulated the expression of miR-33a-5p, enhanced the sensitivity of EC cells to MPA and potentially exerted anticancer effects in EC through the synergistic action of the miR-33a-5p/FBXL16 axis in combination with MPA.

In conclusion, the identification of specific miRNAs as predictors of TTFT holds promise for enhancing risk stratification in CLL to predict therapeutic needs. However, further validation studies and in-depth functional analyses are required to confirm the robustness of these observations and to facilitate their translation into meaningful clinical utility.

HDAC1/FOXK1 upregulation and miR-33a silencing are new mechanisms of EGFR-TKI resistance in NSCLC.