MYO16 (Myosin XVI)

P=N/A, N=35, Completed, King Saud University | Trial completion date: Jan 2026 --> Sep 2025 | Trial primary completion date: Nov 2025 --> Apr 2025 | Recruiting --> Completed

Notably, we identified MICAL2 as a key downstream effector, whose downregulation induces similar consequences observed upon MYO16-AS1 downregulation, suggesting that MICAL2 is a major mediator of the functional effect of MYO16-AS1 in OC. Strikingly, MICAL2 inhibition markedly reduced proliferation accross several OC patient-derived tumor organoid models, regardless of their response to chemotherapy, thereby underscoring MICAL2 as a promising therapeutic target in OC.

The study presents a novel prognostic model based on 14 autophagy-related LncRNAs for patients with lung adenocarcinoma. This model may further guide the clinical treatment of lung adenocarcinoma.

P=N/A, N=40, Recruiting, King Saud University | Trial completion date: Jan 2025 --> Jan 2026 | Trial primary completion date: Nov 2024 --> Nov 2025

Despite significant heterogeneity among the included studies and the use of subjective visual methods for phenotype assessment, our review highlights the critical role of fundamental biological processes, such as development and cellular organisation, in skin ageing. Future research that targets the same SNP across multiple populations could strengthen the association of additional loci with skin ageing. Further investigation into these underlying biological processes would significantly advance our understanding of the pathogenesis of skin ageing phenotypes.

The progression-free survival curves of the TCGA cohort were significantly discriminated by STS-RRI (p = .013) but not by RSI (p = .241). We developed the STS-RRI to predict the radioresistance of patients with STS in the TCGA dataset, showing a higher performance than RSI.

This study demonstrated a proof of principle strategy to identify risk variants found by GWAS, and identified ten candidate loci that could be associated with colorectal, gastric- and prostate cancer.

P=N/A, N=40, Recruiting, King Saud University

IDCP sites also showed increased hypoxia markers HIF1A, BNIP3L, PDK1, and POGLUT1; decreased fibroblast markers COL1A2, DCN, and LUM; and decreased immune cell markers CCR5 and FCGR3A. Overall, these findings indicate that the hypoxic tumor microenvironment and reduced recruitment of fibroblasts and immune cells, which reflect morphological features of IDCP, may influence the aggressiveness of high-grade prostate cancer.

Heritability is enriched in regions with increased chromatin accessibility in adult oligodendrocytes (as well as microglia, inhibitory neurons and astrocytes) and multiple fetal cell types, suggesting that genetic control of structural connectivity is partially mediated by effects on myelination and early brain development. Our results indicate pervasive, pleiotropic, and spatially structured genetic control of white-matter structural connectivity via diverse neurodevelopmental pathways, and support the relevance of this genetic control to healthy brain function.

Furthermore, we found that MYO16-AS1 competitively bound to the IGF2BP3 protein and in turn reduced IGF2BP3 protein binding to HK2 mRNA, decreasing HK2 mRNA stability and inhibiting glucose metabolism reprogramming and LUAD cell invasion in vitro and in vivo. The finding that the MYO16-AS1/IGF2BP3-mediated glucose metabolism reprogramming mechanism regulates HK2 expression provides novel insight into the process of LUAD invasion and suggests that MYO16-AS1 may be a therapeutic target for LUAD.

This study revealed distinct molecular landscapes of different subtypes of TETs, suggesting diverse pathogenesis of non-B3 thymomas, B3 thymomas, and TCs. Our findings warrant further validation in future large-scale studies and may provide a theoretical basis for potential personalized therapeutic strategies.