TP53INP1 (Tumor Protein P53 Inducible Nuclear Protein 1)

Finally, starvation enhances TP53INP2 translation via the m6A demethylase FTO, without altering mRNA stability. These findings uncover coordinated regulation of TP53INP2 localization and turnover by cellular stress.

Given the modest, single-center sample size and lack of external validation, these findings should be considered exploratory. Larger, multi-center validation studies are essential before clinical translation.

Collectively, this study highlights the critical role of TP53 target genes in the immediate response of TNBC cells to DNA-damaging agents like doxorubicin and etoposide. It also reveals distinct molecular mechanisms regulating their expression in resistant versus sensitive cells, offering potential therapeutic targets to improve treatment strategies for TNBC.

Driver coefficients for TP53INP1, CA12, and CCNL1 aligned with known biology, and epithelial drivers exerted measurable influence on NK cells, consistent with their stage-wise decline. By leveraging temporal single-cell structure, CancerTrace transcends the static and cohort-dependent limitations of existing tools, inferring causal, time-directed driver-modulator relationships that advance mechanistic understanding and precision oncology.

EZH2 deficiency effectively enhances the chemosensitivity of DLBCL cells to Glofitamab, manifested by promoting Glofitamab-mediated inhibition in the proliferation, migration, and invasion of DLBCL cells...In summary, EZH2 inhibits the progression of DLBCL via driving H3K27me3 methylation of TP53INP1. Targeting EZH2 may be a promising strategy for DLBCL.

We confirm that miR-92a-1-5p regulates proliferation and cell cycle by targeting TP53INP1 and decreases autophagy by targeting BNIP3L. Our data suggest that miR-92a-1-5p plays a role in CML progression, and its inhibition enhances imatinib anti-leukemic efficacy, making it a potential therapeutic target.

These findings suggest that this miRNA signature has potential to be used as a diagnostic and prognostic biomarker and could serve as a foundation for future therapeutic strategies for endometrial cancer. However, further experimental validation is needed to confirm its clinical applicability.

ENST00000523905 could recruit and directly bind with CCAAT/enhancer (C/EBPβ), which can promote the expression of TP53INP1. Taken together, our findings demonstrated that ENST00000523905 may increase autophagy via enhancing TP53INP1 expression through binding with C/EBPβ, resulting in oxidative stress-induced decrease in ECM in HTMCs.

We demonstrate that miR-155 deficiency impairs cell proliferation, cell cycle, transcriptome, and miRNome via deregulation of the MIR155HG/TP53INP1/CDKN1A/CCND1 axis. Our CLL model is valuable for further studies to manipulate miRNA levels to revert highly aggressive leukemic cells to nearly benign or non-leukemic types.

Silence of TP53INP1 reversed the effect of miR-3154 knockdown on proliferation and metastasis of glioblastoma cells. These findings show that miR-3154 promotes glioblastoma proliferation and metastasis via targeting TP53INP1.

A deeper understanding of these mechanisms may unveil potential targets for early diagnosis, prognosis assessment, and dietary recommendations for pancreatic cancer. These findings hold clinical significance not only for pancreatic cancer but also for other malignancies exhibiting heightened ZIP4 expression.

Flow cytometry and immunofluorescence showed that oxaliplatin and 5-fluorouracil caused CRT exposure in all models. RNA sequencing identified enrichment of p53 signaling pathway genes, including TP53I3, TP53INP1, and YPEL3, which were confirmed by RT-qPCR. These results suggest that the p53 signaling pathway plays an important role in CRT exposure induced by anticancer drugs.