MIAT (Myocardial Infarction Associated Transcript)

The results of the analysis for the saliva samples suggest a satisfactory diagnostic value for ITGB8 but nonsignificant diagnostic value for the MIAT-lncRNA. ITGB8 and MIAT-lncRNA expression levels could be considered in the evaluation of suspicious oral cavity lesions, especially in the tissue and blood samples.

Race/ethnicity, MED12 mutations, and ovarian steroids influence the expression of ncRNA expression, further implicating their relevance to fibroid pathogenesis. Therapeutic targeting of these dysregulated ncRNAs in fibroids could enable more precise and individualized non-hormonal-based treatment for this common gynecologic tumor.

These findings indicate that lncRNA expression in fibroids is modulated by menopausal status, likely reflecting hormonal influence. Hormone-responsive lncRNAs may play key roles in fibroid pathogenesis and represent potential targets for therapeutic intervention.

Our study demonstrates that the MIAT/JAK3/STAT3 pathway plays a critical role in malignant progression and immune escape of RCC through regulating CD8+ T-cell exhaustion, suggesting its potential as a therapeutic target for RCC immunotherapy.

We also validated that some NetLnc-based predictions could better effectively predict ICI response compared to single molecules using three kinds of machine learning algorithms following independent datasets. Taken together, this study presents the use of a network-based framework to efficiently select ICP-related lncRNAs, which contributes to a comprehensive understanding of lncRNA functions and accelerates the discovery of lncRNA-based biomarkers in ICI treatment.

In conclusion, this study demonstrated that XPD recruited P53 to regulate the MIAT/miR-29a-3p/COL4A1 axis, which contributed to inhibiting migration, invasion, EMT, and metastasis of HCC. Thus, XPD may be a valuable target for HCC treatment.

Dysregulated lncRNAs MIAT and Gm15441 in CRC can be more clinically important in cases of cancer related to UC due to their biological function in regulating the inflammation process, providing new ideas about the diagnosis and management of pyroptosis-related diseases.

As a result, MIAT is thought to be a possible biomarker and therapeutic target for cancer patients. The biological functions, mechanisms and potential clinical implications of MIAT during carcinogenesis and finally the current possible therapeutic approaches targeting MIAT are also outlined in this review.

In conclusion, our findings indicate a significant role for the TNF gene and associated lncRNAs, such as lncRNA MIAT and lncRNA NEAT1, in podocyte apoptosis and the development of DN.

Results demonstrated that MALAT1 knockout significantly reduced MALAT1 expression and attenuated Smad2/3-mediated fibrosis by decreasing pSmad2, pSmad2/3, Smad4, vimentin, fibronectin, collagen-I, and α-SMA expression levels, while increasing Smad7, Smurf2, and E-cadherin levels. These findings suggest that targeting the MALAT1/Smad2/3 pathway could be a potential therapeutic target for mitigating fibrosis to prevent AKI-to-CKD transition.

TQ also affected p53 downstream targets, maintaining p53 levels. This study elucidates the anti-cancer mechanisms of TQ in A172 GBM cells, underscoring its effects on multiple signaling pathways and positioning TQ as a promising candidate for innovative glioblastoma treatment strategies.

Furthermore, through Cox regression analysis and three machine learning models, we identified 11 key methylation-driven lncRNAs (DIO3OS, ELOVL2-AS1, MIAT, LINC00536, C9orf163, AC105398.1, LINC02178, MILIP, HID1-AS1, KCNH1-IT1, and TMEM220-AS1) that were associated with the survival of breast cancer patients and constructed a prognostic risk scoring model, which demonstrated strong prognostic performance. These findings enhance our understanding of DNA methylation's role in lncRNA regulation in breast cancer and provide potential biomarkers for diagnosis.