These findings suggest that MIR31HG polymorphisms rs72703442 and rs55683539 may confer a protective effect against BC in this population, although no association with clinical features was observed. Larger multiethnic studies are needed to validate these associations and clarify underlying mechanisms.
In addition, we also discuss the potential of lncRNAs as therapeutic targets for HCC, such as: lncRNA MIR31HG, CASC2c, and lncRNA AC115619. Furthermore, we also explore the application prospects of lncRNAs as potential biomarkers and therapeutic targets, providing new perspectives and directions for future HCC research.
The complex regulatory networks involving lncRNAs provide new insights into psoriasis pathogenesis and offer promising avenues for personalized treatment strategies. Integration of lncRNA profiling into clinical practice may enhance our understanding of disease heterogeneity and improve therapeutic outcomes for psoriatic patients.
Functional assays demonstrated that CIC structure formation substantially augmented the malignant properties of Cal27 cells, including increased resistance to both cisplatin and gemcitabine. This mechanism promotes HNSCC cell survival, fosters an immunosuppressive microenvironment, and drives chemoresistance. Therefore, targeting MIR31HG represents a viable therapeutic avenue to disrupt immune resistance and enhance chemosensitivity in HNSCC.
Our results indicate that MIR31HG is crucial in regulating PDAC progression, particularly in the aggressive basal-like subtype associated with hypoxia and partial EMT. Targeting the MIR31HG-mediated network may offer a novel therapeutic approach to combat hypoxia-driven PDAC.
This study successfully established a LUAD risk scoring model composed of 12 ferroptosis-related genes. In the future, this model is expected to be used in conjunction with the tumor-node-metastasis (TNM) staging system for prognostic predictions in LUAD patients.
This regulatory interplay underscores the therapeutic potential of ncRNA-targeted strategies to restore p16INK4a function. We summarize recent studies supporting that ncRNAs that control p16INK4a may be diagnostic biomarkers and therapeutic targets for age-related diseases and cancer.
Consistently, in vivo studies showed that the knockdown of MIR31HG or RIPK4 reduced tumor size in xenograft animal models. The roles of lncRNA MIR31HG in breast cancer were associated with its regulatory effects against RIPK4.
In vivo MIR31HG repression with an antisense oligonucleotide attenuated tumor growth and distal organ metastasis, whereas MIR31HG promotion remarkably encouraged cellular invasion in lung and liver tissues. Our data suggested that MIR31HG is a potential diagnostic indicator and druggable therapeutic target to facilitate multiple strategic treatments for lung cancer patients.