SNHG12 (Small Nucleolar RNA Host Gene 12)

SNHG12 knockdown inhibits DTX resistance of PCa cells by reducing SNHG12 binding to ELAVL1 to inhibit the activation the PI3K/AKT signaling pathway.

FAM171A2 demonstrates context-dependent expressions that are modulated post-transcriptionally in gynecologic cancers. While it is not independently prognostic, it may serve as a molecular hub at the intersection of neuronal and immune pathways, warranting further mechanistic investigations and exploration as a panel-based biomarker.

Overall, SNHGs may serve as molecular biomarkers and hold potential therapeutic target value. However, existing evidence is largely based on in vitro and small-sample studies, requiring further validation in clinical cohorts and functional models.

In our experimental models, SNHG12 silence suppresses, while ectopic expression of SNHG12 expedites, Erastin- and RSL3-induced ferroptosis. Consequently, SNHG12 restrain the antioxidant response of NRF2 to elevate the intracellular labile iron pool and accelerate GSH exhaustion in response to pro-ferroptotic insults, thereby modulating ferroptosis susceptibility in cancer cells. Collectively, our findings propose a novel regulatory circuit modulating ferroptosis, comprising SNHG12-TRIM25-KEAP1, and highlight the potential application of manipulating this regulatory axis in cancer treatment through ferroptosis.

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 results showed the BC subtype-specific expression profiles of SNHG12 and HAGLR and represent these lncRNAs as useful diagnostic and prognostic biomarkers for BC.

Additionally, APS demonstrated significant antioxidant effects. Therefore, APS can inhibit oxidative stress and suppress NPC progression by targeting the SNHG12/miR-30a/AKT3 signaling pathway.

Mechanistically, RIP and ChIP assays revealed that SNHG12 interacts with HMGB1 and inhibits PTEN transcription by preventing HMGB1 from binding to the PTEN promoter, thereby promoting glycolysis in KGN cells. Our findings collectively demonstrate that the SNHG12/HMGB1/PTEN axis serves as a novel regulatory mechanism in PCOS by modulating glycolytic-mediated follicular dysplasia in GCs, offering a potential therapeutic target for PCOS.

Collectively, results of the present study revealed that SNHG12 suppressed ferroptosis and promoted the metastasis of NSCLC, further demonstrating that high SNHG12 expression levels may be indicative of poor clinical outcomes for patients with NSCLC. Thus, the present study highlighted that the SNHG12/miR-326/SLC7A11 axis may exhibit potential as a novel target for the treatment of NSCLC.

SNHG12 promotes EMT and metastasis of CRC by modulating the TGF-β/Smad2/3 signaling pathway and EMT process, which could function as a prognostic biomarker and a treatment target for CRC.

In addition, this review provides insights into the development of specific probes, including fluorescent, electrochemical, and radionuclide probes, for sensitive and accurate detection of prostate cancer biomarkers. In conclusion, this review provides a comprehensive overview of the status and future directions of prostate cancer biomarker research, emphasizing the potential for precision diagnosis and targeted therapy.