KCNQ1OT1 (KCNQ1 Opposite Strand/Antisense Transcript 1)

KCNQ1 is a tumor suppressor of CRC that is DNA methylated. DHZCP in combination with KCNQ1 overexpression exhibits anti-CRC effects through the regulation of cuproptosis-related pathways, cuproptosis is promoted, oxidative stress is enhanced, and copper accumulates, thus supporting the clinical application prospects of DHZCP in CRC.

Through integrated multi-omics analysis, we established that oxidative stress pathways may drive pNET progression through a coordinated mechanism involving metabolic reprogramming (via BCL2L1 and PHGDH downregulation), immune microenvironment remodeling (through altered dendritic cell and NK cell function), and complex regulatory networks. BCL2L1 and PHGDH represent potential diagnostic biomarkers and candidate therapeutic targets that require experimental validation, providing new directions for precision medicine in pNET.

This study developed an integrated microfluidic platform for rapid EV isolation and established an EVlncRNA Score model, enabling highly efficient early HCC detection, even in AFP-negative cases. A multiparametric diagnostic model further improved accuracy, offering a promising tool for clinical HCC screening. This strategy presents a robust, non-invasive liquid biopsy strategy with significant potential for early HCC detection.

Patients in moderate stages were primarily associated with the EMX2OS score. The research findings demonstrate that the nine-lncRNA signature, when combined with deep learning, offers a powerful approach for recurrence risk stratification in cervical cancer.

PDK4 functions as a tumor suppressor in GC, bridging metabolic reprogramming, epigenetic regulation, and immune microenvironment remodeling. Its downregulation contributes to disease progression and immune evasion, underscoring its potential as a prognostic biomarker and therapeutic target. Restoring PDK4 activity may serve as a promising strategy to mitigate GC aggressiveness and therapeutic resistance.

Notably, bezafibrate, a PPAR pan-agonist, demonstrated substantial genetic overlap with T2D loci, supporting its potential in metabolic disease. This study introduces a genetically informed pipeline for drug repurposing based on multi-trait gene set analysis.

In summary, the current study provides an extensive ceRNA network that highlights novel prognostic biomarkers for stomach adenocarcinoma.

A total of 41 drugs were predicted to have potential therapeutic effects, including omarigliptin, bepridil and bortezomib. Finally, qRT-PCR validation demonstrated that SLC26A4, KCNQ1, PMAIP1, DPP4, and NOX4 had expression trends consistent with public database results. This study identified 6 MDRGs (SLC26A4, SLC25A37, KCNQ1, PMAIP1, DPP4 and NOX4) associated with the prognosis of DDTC, providing valuable scientific insights and references for the targeted therapy and patient stratification of DDTC.

This study demonstrates that the BWS patients with MLID exhibit highly variable methylation changes that affect both imprinted and non-imprinted loci in a seemingly stochastic manner throughout the genome. These findings support the hypothesis that MLID results from the interaction of maternal-effect genes and environmental factors in aged oocytes, leading to disordered DNA methylation in the whole genome. Future research should investigate whether and how these epimutations impact the health of affected individuals, particularly in adulthood.

Single-cell RNA sequencing demonstrated that CACNA1C was expressed in fibroblasts and myofibroblasts, PIEZO1 was expressed across all five cell subtypes, and TRPV4 was expressed in fibroblasts and monocytes or macrophages. This study initially identified unique molecular subtypes and key genes for patients with OC from the novel angle of MICs.