MIR210HG (MIR210 Host Gene)

A prognostic model concerning disulfidptosis-related lncRNAs was constructed to predict outcomes in HCC. This model provides insights into molecular mechanisms, characterizes the tumor microenvironment, and predicts patient responses to immunotherapy and targeted treatments.

Mechanistically, we elucidated that MIR210HG promoted the malignant phenotypes of TNBC by upregulating the expression of HIF-1α protein, which in turn initiated RASSF7 transcription, resulting in the promotion of epithelial-mesenchymal transition (EMT) process. Collectively, our results identified MIR210HG as a key molecule mediating exosome-based communication from hypoxic TAMs to TNBC cells and revealed its pro-metastatic role, Consequently, MIR210HG emerges as a highly promising therapeutic target of TNBC.

This study highlights the CREB3-MIR210HG axis as a pivotal mechanism driving CC cell proliferation. Targeting this regulatory pathway may provide a novel therapeutic strategy for CC treatment, with the potential for developing lncRNA-based therapies aimed at inhibiting this axis to slow down tumor growth and progression.

MIR210HG emerges as a pivotal gene in ESCC, influencing both the immunity and prognosis of patients. Moreover, it may affect autophagy and apoptosis via the P53 signaling pathway. Overall, these outcomes present novel ideas for ESCC treatment.

The findings suggest that lncRNA MIR210HG contributes to hepatocellular carcinoma progression by regulating autophagy and could serve as a promising therapeutic target in hepatocellular carcinoma treatment strategies.

MIR210HG promotes colon cancer cell proliferation by binding to PCBP1 and inhibiting ferroptosis. These findings suggest MIR210HG as a potential therapeutic target for colon cancer.

lncRNA MIR210HG accelerated the progression of colorectal cancer by controlling miR-1226-3p. lncRNA MIR210HG/miR1226-3p may potentially serve as therapeutic targets for addressing colorectal cancer.

AC099850.3 accelerates the cell cycle progression and promotes the occurrence and development of HBV-HCC by upregulating immune checkpoint CD276 expression. CC@AC&SF@PP NPs loaded with AC099850.3 siRNA and SF improve the effectiveness of combined therapy for HBV-HCC.

Finally, we validated the accuracy of FCRLs in hepatocellular carcinoma cell lines using induction agents (elesclomol and erastin). Cellular assays revealed significant changes in the expression of AC019080.5, AC145207.5, MIR210HG, and LINC01063 in HCC cell lines following the addition of ferroptosis and cuproptosis inducers. We created a signature of four FCRLs that accurately predicted survival in HCC patients, laid the foundation for basic research related to ferroptosis and cuproptosis in hepatocellular carcinoma, and provided therapeutic recommendations for HCC patients.

In addition, we established both in vivo and in vitro models of HPH to validate the differential expression of specific markers associated with hypoxia. Our findings suggest a potential mechanism of LncRNA MIR210HG in the progression of HPH and offer potential targets for disease intervention and treatment.

We established a GILncSig that can predict the prognosis of HCC patients, which will help to guide prognostic evaluation and treatment decisions.

A first pan-can cancer analysis of MIR210HG highlights its transcriptional and epigenetic deregulation and oncogenic role in the majority of cancers, its correlation with tumor microenvironment factors such as hypoxia and immune infiltration, and its potential as a prognostic biomarker and therapeutic target in several cancers.