HOXA10 (Homeobox A10)

Roc curve analysis revealed that the diagnostic power of HOXA10-AS was high (AUC = 0.64) in the tumor compared to the normal GC tissues. Our findings show that HOXA10-AS expression level is higher in the GC tumor compared to the adjacent non-carcinoma tissues and can act as a strong diagnostic biomarker in GC patients.

This five-gene signature represents a biologically interpretable biomarker panel with potential utility for immunotherapy response stratification in HCC. The integrative analytical framework provides preliminary evidence supporting its value, warranting further validation in larger, independent clinical cohorts before clinical translation.

Four antisense genes, namely HOXA10-AS, LEF1-AS1, MSC-AS1, and ZEB2-AS1, have been clinically cross-validated and have consistently demonstrated to be associated with patient outcomes in multiple independent cohorts by different research teams, with clear evidence for the prioritization of clinical biomarker development in HNC. Single nucleotide polymorphisms (SNPs) of antisense genes with evidence for HNC risk or outcomes should be further validated in different ethnic groups, for potential global HNC applications.

Taken together, we concluded that ALKBH5-induced m6A demethylation increased the stability and expression levels of NEAT1, and elevated NEAT1 facilitated cancer progression in HNSCC through regulating the downstream miR-654-3p/HOXA10 axis. This study provided potential biomarkers for the diagnosis, treatment and prognosis of HNSCC in clinic.

Collectively, this study reveals that recombinant human granulocyte colony-stimulating factor (rhG-CSF) improves implantation partly by downregulating hsa_circ_0001550. These findings provide new perspectives for understanding implantation mechanisms and developing therapeutic strategies.

The reduced tumorigenic behavior of glioblastoma cells due to HOXA10-AS knockdown can be rescued by ITGB5 overexpression or miR-99a-3p inhibitor. These results indicate that HOXA10-AS promotes tumorigenic behavior in glioblastoma cells by regulating the EMT-like process and functioning as an miR-99a-3p sponge to modulate ITGB5 levels, providing insights into glioblastoma development and potential therapeutic targets.

Finally, integrative analyzes demonstrated strong correlations between promoter accessibility, transcription factor occupancy, and gene expression, and uncovered cooperation between epigenetic and genetic drivers. Together, these findings reveal context-dependent functional hierarchies among HMEs and underscore the necessity of multi-layered analyses to resolve the complexity of epigenetic regulation in cancer.

Lnc5q21.2 promotes ATR pathway by activating Wnt signaling via interacting with HOXA10. Lnc5q21.2 sensitizes CRC cells to ATR inhibitor both in vitro and in vivo.

Clinically, these alterations are associated with abnormal uterine bleeding, subfertility, implantation failure, miscarriage, pregnancy complications, and postmenopausal endometrial hyperplasia and cancer. Overall, our review provides novel insights into the molecular mechanisms linking systemic metabolic and endocrine dysfunction with endometrial pathology in PCOS and has broader implications that apply to all women.

This review consolidates the current body of knowledge regarding the epigenetic regulation of endometrial receptivity. It outlines fundamental scientific data on epigenetic mechanisms and discusses contemporary diagnostic and pharmacological intervention strategies.

Our analysis identifies METTL3 as a central node in GC's molecular landscape, bridging epigenetic dysregulation with malignant phenotypes and therapy failure. These insights not only redefine METTL3's role in GC but also provide a roadmap for targeting m⁶A machinery in precision oncology.

Conclusions Patients with thin endometria showed improvement in EMT, histoarchitecture, and receptivity genes after AB and AB+Cells intervention. Implications The study demonstrates the potential of using a 3D amnion bilayer scaffold with endometrial cells to improve endometrial regeneration.