Moreover, there was interaction between METTL3 and LINC00857. METTL3-mediated N6-methyladenosine modification of LINC00857 enhanced metastasis and stemness of OC cells via activating the YAP-TEA domain transcription factor pathway.
Notably, this tissue-based biomarker panel robustly discriminated precancerous lesion and cervical cancer patients from non-disease controls in a blood-based validation set (30 normal, 25 HSIL and 50 cervical cancer) with an AUC value of 0.9320. This study presents a non-invasive, efficient diagnostic panel for cervical cancer screening.
NNK potentially induces PC progression through the LINC00857/β-catenin axis. These findings provide new perspectives on the mechanisms of PC progression and highlight the clinical relevance of smoking cessation for preventing PC.
Our results identified promising biomarkers that play a role in specific groups of prostate cancer patients. Detecting specific biomarkers may be an effective strategy for different groups of PC patients.
Furthermore, the tumor-promoting effects induced by low-dose OXA were notably suppressed through LINC00857. Evidence from this study indicates that apigenin can effectively suppress the metastasis of OSCC cancer cells induced by low-dose OXA through inhibiting the level of LINC00857, suggesting a promising therapeutic strategy.
Subsequently, the downstream factors, miR-486-5p and NEK2, were screened, and the putative regulatory axis was examined. Overall, the regulatory effect of methylation-mediated LINC00857 overexpression on miR-486-5p/NEK2 axis may be a new mechanism for LUAD progression.
By integrating multi-omics data, we identified four core sialylation-related lncRNAs and successfully established a prognostic model to distinguish patients with different characterizations. These findings may provide some insights into the underlying mechanism of sialylation, and offer a new stratification way as well as clinical guidance in LUAD.
Additionally, the FOXP3 inhibitor epirubicin exhibited the ability to impede proliferation and induce ferroptosis in GBM cells both in vitro and in vivo. In summary, our study provided evidences that FOXP3 facilitates the progression of glioblastoma by inhibiting ferroptosis via the linc00857/miR-1290/GPX4 axis, highlighting FOXP3 as a potential therapeutic target for GBM.
Furthermore, ceRNA network analysis suggested the involvement of the LINC00857/has-miR-1179/DLAT axis in the development of PAAD. Overall, this study provides theoretical support for the investigation of diagnostic and prognostic biomarkers as well as potential therapeutic targets in PAAD.
The novel 5-NRL signature is helpful for assessing the prognosis of PC patients and improving therapy options, so it can be further applied clinically.