MEOX2 (Mesenchyme Homeobox 2)

Using a GLICO (GLioblastoma Cerebral Organoid) model, we show that MEOX2 knockdown impairs tumor growth and increases sensitivity to temozolomide (TMZ)...Consistent with this, MEOX2-depleted cells exhibit reduced PARylation levels and increased sensitivity to the PARP1 inhibitor Talazoparib, highlighting a potential therapeutic vulnerability. Altogether, our findings reveal a previously unrecognized role for MEOX2 in the DNA damage response of GSCs, particularly in promoting survival and recovery after chemotherapy and ionizing radiation. These results also suggest that MEOX2 functions as a partner of PARP1 and may represent a promising therapeutic target in GBM.

Allogeneic hematopoietic stem cell transplantation was associated with better survival, underscoring its significance. These findings reveal the genetic and clinical heterogeneity of NUP98-rearranged AML in adults and support its classification as a distinct entity, highlighting the need for fusion partner-specific therapeutic strategies.

These defects sensitized cells to radiation and decreased clonogenic survival after ionizing radiation and PARP inhibition. Ppm1d mutations confer intermediate suppression of the p53 pathway, consistent with the clinical features of PPM1D -mutant DMGs and are associated with radiosensitivity and PARP inhibitor vulnerability.

Prognostic models based on tumor microenvironment and immune score stratification and the construction of related genes have potential applications for prognostic analysis of GBM patients.

After being treated with the oxidative stress inducer H2O2 and the antioxidant N-acetylcysteine (NAC), cell viability, reactive oxygen species (ROS) levels, adhesion, and transendothelial migration of MCF7 and MDA-MB-231 cells to HLEC cells were detected...Overexpression of MEOX2 resulted in smaller tumor volume, lower ROS levels, and lower CXCR4 and CCR7 expression levels. MEOX2 and RGS5 are pivotal in regulating breast cancer metastasis, offering valuable insights into potential therapeutic strategies for breast cancer metastasis.

The developed prognostic signature and nomogram offer practical tools for risk stratification in clinical settings, with IGFBP2 identified as a promising therapeutic target. These insights highlight the potential of palmitoylation-focused therapies to enhance outcomes for LGG patients.

The developed nomogram model effectively visualizes and accurately predicts patient prognosis. It is essential to highlight that individuals diagnosed with low-risk metastatic KIRC may experience greater advantages from the administration of immunotherapy and sorafenib.

In vivo experiments demonstrated that circ_0000190 overexpression significantly reduced tumor volume and weight (P<0.001), concomitant with elevated MEOX2 mRNA and protein levels (P<0.001) and decreased miR-301a expression (P<0.001). In conclusion, our study elucidates that circ_0000190 suppresses TNBC progression by downregulating miR-301a and upregulating MEOX2, forming a competitive endogenous RNA (ceRNA) network of circRNA-miRNA-mRNA.

Combined CL and MES GSCs targeting demonstrates enhanced efficacy, both in vitro and in vivo. Our results highlighted a therapeutic strategy for the elimination of heterogeneous GSCs populations through combinatorial targeting of MEOX2 and SRGN in GSCs.

It may confer cisplatin resistance to OV cells by activating the E2F target and DNA repair pathway to mitigate cisplatin-induced early apoptosis. Despite certain limitations, these findings provide novel insights into the potential role of MEOX2 as a prognostic biomarker and therapeutic target in OV.

Furthermore, our results suggest that BRD9 may contribute to the activation of both lung cancer oncogenes GLI-1 and EGFR. Such findings suggest that SMARCB1 and MEOX2 could serve as important prognosis biomarkers and target genes in human lung cancer therapy, offering new opportunities for the development of more effective and selective treatment strategies in the field of lung malignant diseases.

This investigation illuminates the critical potential of targeting CAFs to augment immunotherapeutic approaches in prostate cancer. Our findings contribute to a deeper understanding of the TME's complexity, advocating for further exploration into CAF-targeted therapies aimed at enhancing treatment responses and ultimately improving patient outcomes.