ZMAT3 (Zinc Finger Matrin-Type 3)

ZMAT3 depletion resulted in increased JUN binding at the HKDC1 promoter and increased HKDC1 transcription that was rescued upon JUN depletion, suggesting that JUN activates HKDC1 transcription in ZMAT3-depleted cells. Collectively, these data reveal a mechanism by which ZMAT3 regulates transcription and demonstrates that HKDC1 is a key component of the ZMAT3-regulated transcriptome in the context of mitochondrial respiration regulation.

Accordingly, combined Zmat3-Cdkn1a inactivation dramatically enhanced cell proliferation and migration compared to controls, akin to p53 inactivation. Together, our findings place ZMAT3 and CDKN1A as hubs of a p53-induced gene program that opposes tumorigenesis across various cellular and genetic contexts.

Nab-paclitaxel significantly upregulated phosphorylated AMPKα, apoptotic proteins as zinc finger matrin-type 3, and nuclear factor kappa-B levels following radiation exposure. Our study confirmed the radiosensitizing effect of nab-paclitaxel on cholangiocarcinoma cells through a dual effect of antitumor proliferation and inhibition of M2 macrophage polarization, and the underlying mechanism involved activation of the AMPK signaling pathway.

Silencing the ZMAT3 gene in the TSPRS significantly reduced the proliferation and invasiveness of breast cancer cells. Our study developed a TSPRS, which emerges as a potent predictive instrument for the prognosis of breast cancer, offering novel perspectives on the immunotherapeutic approach to the disease.

Accordingly, combined Zmat3 - Cdkn1a inactivation dramatically enhanced cell proliferation and migration compared to controls, akin to p53 inactivation. Together, our findings place ZMAT3 and CDKN1A as hubs of a p53-induced gene program that opposes tumorigenesis across various cellular and genetic contexts.

Furthermore, some of these genes were central to PCa occurrence, with BBC3 also influencing progression and prognosis. Importantly, BBC3 expression was upregulated in clinical PCa samples and affected PCa cells sensitive to olaparib, suggesting its potential as a predictive marker for PCa development and olaparib resistance.

Our findings suggest that ZMAT3 is a prognostic biomarker linked to immune invasion in breast cancer. Elevated ZMAT3 expression correlates with adverse clinical outcomes, indicating its potential role in disease progression.

These include ZMAT3, GLS2, PADI4, ZBXW7, RFX7, and BTG2. The findings from these studies provide a more complex, but exciting, potential framework for understanding the role of p53 in tumor suppression.

Conclusions   NFE2L2 mutations display notable heterogeneity in lung cancer. The coexistence of NFE2L2 mutations and 3q26 amplification warrants in-depth exploration of their potential clinical implications and treatment approaches for affected patients.

This analysis suggests that in addition to ZMAT3 loss, additional TRP53-regulated processes must be disabled simultaneously for TRP53-mediated tumour suppression to fail. Our findings reveal that the absence of different TRP53 regulated tumour suppressive processes changes the tumour spectrum, indicating that different TRP53 tumour suppressive pathways are more critical in different tissues.

Moreover, the expression levels of the seven SOSCRGs in five different breast cancer cell lines were quantified and compared by qPCR respectively. Multidimensional evaluations verified the clinical utility of the SOSCRGs-based predictive model to predict prognosis, aid clinical decision, and risk stratification for patients with breast cancer.

Furthermore, a manual bibliographic search for each gene was carried out, and a Protein-Protein Interaction (PPI) network was built to verify existing associations among them, followed by a new enrichment analysis. The results revealed that all the genes are highly relevant in the context of thyroid cancer and, more particularly interesting, PTGFR and DPP6 have not yet been associated with the disease up to date, thus making them worthy of further investigation as to their relationship to PTC.