PSMD4 (Proteasome 26S Subunit Non-ATPase 4)

Subchronic exposure to an AFB1-dominant AF mixture in rats was associated with iCCA characterized by high proliferative activity, p53 accumulation, and disruption of G1/S checkpoint components. These findings broaden the oncogenic spectrum of AFs and warrant genomic confirmation of AF mutational signatures.

This study highlights the prognostic significance of mitochondrial function-related genes in HCC and establishes a framework for developing innovative diagnostic and therapeutic interventions. Future research should prioritize clinical validation of these findings and evaluate the translational potential of the identified drug candidates in HCC.

Moreover, our NMR relaxation dispersion experiments revealed a dynamic Zn-coordination site in isoforms 1 and 3, but not in isoform 2 of UBE3A, suggesting its possible isoform-specific sensitivity to oxidative stress. This structural and biophysical characterization of the isoforms will advance our understanding of isoform-specific functions of UBE3A and may contribute to future treatment strategies for Angelman syndrome and other UBE3A-related diseases.

Here, we utilize both bacterial infection and a synthetic colibactin analog to identify genes directly involved in colibactin response. These findings provide insight into how differences in gene expression may render certain individuals more vulnerable to colibactin-initiated tumor formation after DNA damage.

Analysis of gene expression by qRT-PCR and differential gene expression revealed that GADD45g genes can be effective genes in the proliferation of oncolytic HSV-1 virus. The transcriptome changes in tumor cells infected by oHSV-1 may be utilized to predict oncolytic efficacy and provide rational strategies for designing next-generation oncolytic viruses.

Our research reveals underlying relationships between metabolic phenotypes and immunological profiles and suggests a unique M2 classification technique for CRC. The identified gene signatures may be key factors linking immunity and tumor metabolism, warranting further investigations.

Our investigative endeavor has highlighted a definitive causative association between genetic inclination to AF and specific digestive system neoplasms, spotlighting IS and HF as instrumental mediators. Such revelations furnish pivotal perspectives on the complex genetic interconnections between cardiovascular anomalies and certain digestive tract tumors, emphasizing prospective therapeutic and diagnostic worthy of pursuit.

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Thus, our findings suggest that PSMD4 is involved in HCC tumor growth through COX2 expression and p53 downregulation. Therapeutic strategies targeting PSMD4 and its downstream effectors could be used for the treatment of PSMD4-abundant HCC patients.

We observed different degrees of abnormal expression of members of PSMD family in ovarian cancer. Among these, PSMD8 was significantly overexpressed in ovarian malignant tissue, and was associated with poor prognosis. PSMDs, especially PSMD8, can serve as potential diagnostic and prognostic biomarkers and therapeutic targets in ovarian cancer.

Subsequently, we assessed the role of PSMB4 and PSMD4 to the sensibility of PI bortezomib in two myeloma cell lines carrying 1q21+...Our study identified proteasome subunits PSMB4 and PSMD4 to be significantly upregulated in SMM and MM patients with 1q21, correlated with 1q21 copy number but not with disease stage. In addition, knockdown of both, PSMB4 and PSMD4 decreased MM cell proliferation. Therefore, targeting PSMD4 could be a strategy to treat patients with 1q21 amplification.

In MM xenograft models, SB was well-tolerated, inhibited tumor growth, and prolonged survival. Our data suggests that inhibiting Rpn10 will enhance cytotoxicity and overcome PI-resistance in MM, providing the basis for further optimization studies of Rpn10 inhibitors for clinical application.