TPR (Translocated Promoter Region)

Moreover, the lack of TPR results in nuclear R-loop accumulation, causing DNA damage and cell cycle arrest as well as subsequent inhibition of cell proliferation in cervical cancer cells. This study highlights the nuclear export of circRNA, lncRNA and mRNA relies critically on TPR, a mechanism that may inhibit nuclear accumulation of R-loop and DNA damage in cervical cancer cells.

Translationally, these findings highlight pathways and targets to promote immune recovery in pediatric cancer patients undergoing cytoreductive therapy. Analytically, this framework advances spatial proteomics by enabling high-confidence protein identification in lymphoid tissues, broadening the potential of translational proteomic research.

The findings indicated that TPR and FGA exhibited good diagnostic performance, with AUCs of 0.946 (p = 0.002; 95% confidence interval [CI], 0.84-1.05) and 0.809 (p = 0.034; 95% CI, 0.65-0.97), respectively. Our results suggest that the TPR and FGA levels are potential predictors of post-EGFR-TKI treatment relapse.

Moreover, a significant disparity in drug sensitivity to AZD8055, paclitaxel, and PD0325901 was noted between the high-risk and low-risk cohorts, and the established four-gene risk signature served as dependable prognostic indicators in the validation cohort, confirmed at the cellular level through external dataset validation and reverse transcription quantitative PCR (RT-qPCR) experiments. A risk signature based on GRGs was established for OS, exhibiting robust predictive efficacy for prognostic assessment, and offering significant clinical utility for the prognosis of OS.

Additionally, we demonstrate the impact of these inhibitors on cellular energy metabolism, and neurite outgrowth, which are subjects of FKBP51 regulation. Overall, the results from this study highlight a novel pharmacological approach towards regulation of FKBP51 function and more generally, Hsp90 function via its interaction with TPR co-chaperones.

According to the in vitro experiments, TPR silencing inhibited the phosphorylation of AKT and the proliferation of HCC cells. In summary, TPR may be a new marker and target for HCC therapy.

It is demonstrated that circZCCHC2 plays a crucial role in the malignant progression of TNBC via the miR-1200/TPR axis, thereby activating the RAS-RAF-MEK-ERK pathway. The present results indicate that circZCCHC2 has the potential to serve as a novel prognostic biomarker for TNBC.

Our findings indicated that NUP133, NUP37, NUP43, NUP50, GLE1 and NDC1 are overexpressed in esophageal carcinoma, among which NUP50 and GLE1genes are reported for the first time in esophageal carcinoma. All identified NUPs were also associated with distant metastasis.Communicated by Ramaswamy H. Sarma.

MKI67, TCHH and TPR were potential prognostic markers for dMMR colorectal cancer. Based on these data and rationale, we suggest that mutations in all exons of these 3 genes should be integrated into predictive biomarker panels for patients with dMMR/MSI-H, aiming to provide more accurate guidance for the selection of personalized diagnosis.

The mRNA levels of multiple hub genes have high diagnostic and prognostic values for TGCT. TPR and PLK4 may play a role in the occurrence and development of TGCT through cancer-related signaling pathways.

The regulation of TPR expression showed similar results. High blood glucose level induced the increase of lncRNA MALAT1 and regulated the expression of TPR by activating miR-7641 to promote the initiation of apoptosis of microvascular endothelial cells, aggravating the neurological dysfunction caused by CSVD.

We further show that NXF1, a well-known mRNA nuclear export factor, associates with tRNAs and mediates their transport through nuclear pores. Collectively, our findings uncover a conserved mechanism that regulates nuclear export of tRNAs, which is a limiting step in protein synthesis in eukaryotes.