SNHG17 (Small Nucleolar RNA Host Gene 17)

The combined four-gene model demonstrated moderate discriminatory power, yielding an AUC of 0.76 (95 % CI 0.65-0.86, p < 0.0001) with balanced sensitivity and specificity of 69.8 % each at the 0.5 cutoff (overall accuracy 69.8 %). Taken together, RUSC1-AS1, SNHG17, PABPC1L and SNHG1 can be novel candidates for future diagnostic studies in CRC.

The candidate biomarker LINC02609 regulates the progression of renal cell carcinoma through the MAPK signaling pathway. The risk model constructed using LINC02609 and SNHG17 was significantly correlated with multiple immunotherapy-related signatures, suggesting that it might be used for the determination of immunotherapy options in KIRC.

The combination of CAF-targeted therapies with immunotherapies or chemotherapy has shown additional potential to reverse this CAF-induced resistance. Autophagy regulation in CAFs can be therapeutic opportunities for novel Interevent strategies.

Our study suggests that STAU1 has oncogenic characteristics and may modulate these genes to influence the proliferation, invasion, and migration of lung adenocarcinoma cells. This research offers new insights that may contribute to the diagnosis and treatment of LUAD.

Specifically, the splice variant SNHG17_2 regulated by RBM10 was upregulated in CRC and was positively correlated with CRC invasion. RBM10 inhibits CRC invasion by regulating the alternative splicing of SNHG17, providing new research directions and potential targets for CRC treatment.

This study contributes to our understanding of the molecular processes driving EC metastasis, which may result in the development of new treatment targets and indicators for the early identification of EC metastasis. More studies are needed to validate these findings and to understand the functional roles of these key factors in EC metastasis.

Although further studies are needed, these data highlight the significant role of SNHGs in tumor biology and the promising potential of this class of transcripts as tools in the clinical management of cervical cancer.

Accordingly, targeting SNHG17 with an anti-sense oligonucleotide (ASO) significantly reduced BCa tumor growth both in vitro and in vivo. Overall, these results established a role for SNHG17 in promoting BCa progression by increasing ATP production and provided insight into the reprogramming of energy metabolism in solid tumors.

Our study identifies four lncRNAs as putative biomarkers with high specificity and accuracy, individually or combined, for differentiating between NAFLD and NASH. Healthy volunteers with PVT1 possess the highest diagnostic accuracy and significantly discriminate between NAFLD and NASH.

We also investigated a possible involvement of genes for these mRNAs in oncogenesis-related processes, such as RNA processing and splicing and epithelial-mesenchymal transition. As a result of this work, four SNHG family lncRNAs with coregulation and joint putative biological functions in the pathogenesis of OC were identified.

Moreover, CCL13-CCR2 axis was identified to be involved in ovarian cancer tumour behaviours driven by oestrogen. There results demonstrate a novel mechanism that exosomal SNHG17 exerts an oncogenic effect on ovarian cancer via the CCL13-CCR2-M2 macrophage axis upon oestrogen treatment, of which SNHG17 may be a potential biomarker and therapeutic target for ovarian cancer responded to oestrogen.

Our research underlines the role of the 6-ferroptosis-lncRNA signature as a predictor of prognosis and a therapeutic alternative for ccRCC.