MIR195 (MicroRNA 195)

This preliminary report highlights a 25-gene deregulated signature in EO-CRC, in which hsa-miR-195 and hsa-miR-549a emerge as biomarkers of clinical relevance, regulating key genes involved in angiogenesis, migration, and invasion. Their dysregulation could contribute to the aggressive clinical features and poor outcomes observed in EO-CRC.

This study identifies distinct miRNA signatures associated with GBC initiation and progression, offering insights into the molecular pathogenesis of the disease. Furthermore, functional studies of the miRNAs implicated in EMT and EGFR-TKI resistance may be conducted using GBC cell lines to dissect the precise roles of key miRNAs and explore their potential as novel therapeutic targets in GBC.

Therefore, these findings suggest that miRNAs may serve as predictive biomarkers and potential therapeutic targets in the management of breast cancer.

Ingenuity Pathway Analysis (IPA) revealed that miR-16-5p and other miRNAs with seed AGCAGCA formed the largest interaction network in GBM, while disease enrichment analysis using Database for Annotation, Visualization, and Integrated Discovery (DAVID) confirmed that the 1000 predicted mRNA targets of DE-miRNAs in GBM were disease relevant. Collectively, these findings identify a robust panel of CSF-derived miRNAs capable of distinguishing IDH-mutant gliomas, GBM, and non-tumor states, supporting the potential of EV-miRNAs as minimally invasive biomarkers for the molecular characterization of diffuse gliomas.

Our study demonstrates that PLOD1, PLOD2, and PLOD3 are significantly upregulated in LIHC and correlate with poor prognosis. The PLOD genes may serve as valuable biomarkers for diagnosis and prognosis in LIHC. Moreover, targeting PLOD genes could provide new therapeutic strategies to hinder tumor progression and metastasis in liver cancer.

Kaplan-Meier survival analysis demonstrated that high expression of hsa-miR-15a (p=0.023) and hsa-miR-221 (p=0.048) significantly correlated with poorer overall survival, suggesting their potential prognostic values. Dysregulated expression of cell-cycle-related miRNAs, particularly hsa-miR-15a and hsa-miR-221, may contribute to CESC progression and serve as potential prognostic biomarkers.

This review delves into the various functions of RFX6, emphasizing its crucial regulatory roles in pancreatic development, tumorigenesis, and progression. In addition, recent advancements in MRS therapy are outlined, underscoring the importance of RFX6-targeted therapy in MRS and cancer.

Metabolomic analyses revealed that CYP4F11 depletion disrupts mitochondrial malate metabolism, while rescue experiments confirmed ME2's pivotal role in mediating CYP4F11's oncogenic effects. Our findings elucidate the CYP4F11/miR-195/ME2 regulatory axis as a crucial determinant of NSCLC progression, highlighting CYP4F11 as both a prognostic indicator and a potential therapeutic target through modulation of cancer cell metabolism.

GO and KEGG enrichment analyses revealed their involvement in pathways related to protein localization, histone binding, and various cancer types. LINC01605 exhibits potential as an EC biomarker, actively regulating carcinogenesis through the ceRNA network, whereas LINC00839 demonstrates a comparatively diminished role in EC diagnosis, sharing common regulatory components.

Rescue experiments indicated that MYB upregulation counteracted the tumor-suppressive effects of miRNA-195-5p and reactivated PI3K/AKT/mTOR signaling. miRNA-195-5p suppresses proliferation and metastasis in TNBC by targeting MYB and inhibiting the PI3K/AKT/mTOR pathway.