PUM1 (Pumilio RNA Binding Family Member 1)

TFRC and 18S rRNA may be suitable RGs in breast cancer tissues, while all five candidates were not stable in adjacent tissues. Larger studies are needed to confirm these findings.

In BJAB B cells, HSUR1 still drives PRE-dependent gene regulation, but the affected genes only partially overlap with those in Jurkat cells, and some transcripts even show reversed direction of change, revealing strong cell-type specificity. By identifying PUM1/2 as key host partners of HSUR ncRNAs, this work uncovers an underappreciated role for PUM proteins in shaping T- and B-cell states and reveals an additional way in which γ -herpesviral ncRNAs reprogram lymphocytes to promote viral persistence.

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None of the animals revealed the expected DGE pattern corresponding to a moderate to high H-ARS-severity degree. Hence, the Göttingen minipig did not qualify as another validation model for our specific gene set, which does not argue against their validity for other purposes.

Despite significant heterogeneity in histology and biological behavior, the shared DNA methylation profile underpins their unified identity. RAD51B-rearranged soft tissue tumors should be included in the differential diagnosis of morphologically undifferentiated or unclassified mesenchymal neoplasms with myogenic differentiation.

PUM1 may serve as a therapeutic target in BC cases with unfavorable prognoses. However, further validation in larger, multi-center cohorts and further functional assessment are required to deepen our understanding of PUM1's role in BC.

This study demonstrates that PUM1 enhances the RNA stability of PAK6, thereby contributing to ferroptosis resistance in LUAD cells.

Notably, inhibition of AP1M2/PUM1-mediated RAD54B expression sensitized BC xenografts to gemcitabine-cisplatin treatment in vivo. These findings unveil a novel mechanism of chemotherapy resistance in BC and highlight the AP1M2/PUM1/RAD54B pathway as a promising therapeutic target to counter resistance and enhance treatment outcomes.

Therefore, this study concludes that the anti-colorectal cancer (CRC) effect of natural metabolites derived from Bifidobacterium longum is limited. Future investigations should focus on refining these natural substances and optimizing their composition ratios to extract their essence while eliminating impurities, thereby obtaining anticancer biologics with exceptional and consistent efficacy.

Expression of the PUM1-TRAF3 fusion was significantly correlated with strong NIK expression, which is associated with a poorer prognosis for patients with BTC. Overall, our study identifies a new fusion gene, PUM1-TRAF3, that activates NIK and non-canonical NF-κB signaling, which may be beneficial for developing precise treatment strategies for BTC.

Our study documents a much broader morphological spectrum of PLAG1-US than previously reported, encompassing but not limited to M-LMS-like morphology with occasional heterologous (particularly adipocytic) differentiation. Since it is currently difficult to precisely define their line of differentiation, for the time being, we suggest using a descriptive name PLAG1-rearranged uterine sarcoma.

This study emphasized the potential of PUM1 as a target for immunotherapy in HCC through TAMs. The present study revealed the molecular mechanism underlying the pro-tumor role of PUM1 in HCC.