SNHG16 (Small Nucleolar RNA Host Gene 16)

High-risk patients were found to be more sensitive to treatment drugs ABT.263, AZD.0530, gefitinib, imatinib, PAC.1, and shikonin. The predictive model we constructed can independently predict the prognosis of patients with CRC. Further experimental validation and mechanistic studies are warranted to elucidate the precise role of OS-related lncRNAs in CRC pathogenesis.

Both bioinformatics analysis and clinical sample validation revealed that high SNHG16 expression in HCC tissues was associated with shorter disease-free survival (HR = 1.711, 95% CI: 1.144-2.559, p = 0.009), higher recurrence rates (p < 0.001), and shorter overall survival (HR = 1.837, 95% CI: 1.283-2.629, p = 0.001). SNHG16 negatively regulates let-7c and serves as a prognostic biomarker for HCC recurrence and survival.

The activity of the lncRNA SNHG16 can be triggered via the hsa-let-7b-5p/AURKA axes. These findings shed light on the novel molecular mechanisms underlying BC progression.

Rescue experiments confirmed that SNHG16-EVs induced NSCLC progression and M2 polarization of THP-1 cells were all reversed by overexpressing miR-132-3p and silencing KIF5A. Collectively, hypoxia-stimulated NSCLC cells transferred SNHG16-containing EVs to promote cancer aggressiveness and M2-polarized macrophages in NSCLC through modulating the downstream miR-132-3p/KIF5A axis, and this study verified that targeting SNHG16-EVs may be a novel strategy to hamper NSCLC progression via modulating TME.

The influence of these regulatory RNAs on the main processes of ovarian oncogenesis, such as apoptosis, epithelial-mesenchymal transition, cell cycle control, and DNA methylation mechanisms in this type of cancer is considered. The prospects for clinical application of regulatory RNAs due to their influence on the level of drug resistance are also discussed.

Our findings demonstrate that SNHG16 and TCF7 lncRNA may act as crucial regulators of the Akt and β-catenin in ALL, which in turn influence c-Myc expression levels in affected individuals. Further research is needed to better understand the molecular mechanisms underlying ALL, potentially leading to improved treatment and monitoring strategies for patients.

The differential expression of disulfide-related genes (DRGs) and DRLs in HNSCC and adjacent normal tissues was further confirmed by qPCR and protein blotting analysis. Our study elucidated the relationship between DRLs and the prognosis, immune microenvironment, tumor mutation burden (TMB), and drug sensitivity of HNSCC and provided new ideas for individualized treatment of HNSCC.

Our findings uncovered that SNHG16 promoted ESCC malignant progression and DDP resistance through the miR-497-5p/HK2 axis, laying the groundwork for deciphering the molecular mechanisms underlying chemotherapy resistance in ESCC and developing new treatment strategies.

However, this overexpression was not associated with any clinicopathological features of HCC patients. In this study, overexpression of ATB and SNHG16 was not associated with survival rate or clinicopathological features of patients with hepatocellular carcinoma.

Lastly, Transwell assay results showed that overexpression of SNHG16/SP1 promoted, while knockdown of SNHG16/SP1 inhibited, the invasiveness of PC-3 and DU145 PCa cells. Collectively, the evidence indicates that the SP1/SNHG16/GLUT1 axis regulates proliferation of PCa cells via the glycolytic route and thus may act as a therapeutic target for PCa treatment.

Moreover, SNHG16 positively regulated the expression of trophinin associated protein (TROAP) by sponging miR-106a-5p in RCC cells, whereas inhibition of miR-106a-5p or overexpression of TROAP greatly reversed the suppression of tumorigenesis and sunitinib resistant by silencing SNHG16. R-exos lncRNA SNHG16 promoted sunitinib resistant and malignant progress by regulating the miR-106a-5p/TROAP axis, and targeting SNHG16/miR-106a-5p/TROAP axis may be a novel therapeutic approach for sunitinib-treated patients of RCC.

&lsqb;This retracts the article DOI: 10.2147/CMAR.S298236.].