TP53TG1 (TP53 Target 1)

In addition, Western blot found that knockdown of TP53TG1 also weakened SMAD3 and JNK1/2 signaling in DPSCs. In conclusion, our study revealed the differentiation-inducing role of TP53TG1 in DPSCs, which plays an important role in dental pulp repair and regeneration and provides new insights and approaches for the prevention and treatment of dental pulp diseases.

This review aims to clarify the expression pattern of TP53TG1 in 10 malignant tumors, its biological relevance, its potential as a therapeutic target, and its importance in clinical applications, thereby offering a novel perspective on molecular targeting in cancer. In the future, integrating TP53TG1 with conventional medications may augment efficacy, offer personalized treatments, and eventually increase the prognosis for patients with aggressive or drug-resistant cancers.

The activation of the transcriptomic network and signaling pathways might be related to the interaction of the characteristic microbiota of the inflammatory disease, with the lung and gut cell receptors present in membrane rafts and complexes. The transcriptomic analysis highlights the impact of several coding and non-coding RNAs, suggesting their relationship with the unlocking of cell phenotypic plasticity for the acquisition of the hallmarks of cancer during lung and gut cell adaptation to inflammatory phenotypes.

Also, its expression decreased after receiving chemotherapy. These findings suggest that PANDA and TP53TG1 expression levels may be possible markers associated with tumorigenesis and may also be considered as possible indicators of response to chemotherapy.

Ultimately, we found that the underlying mechanism involves a competing endogenous RNA regulating network, in which TP53TG1 modulates the target protein STK17B by competitively binding to miR-96-5p, thus regulating glioma progression. These findings suggest that targeting methionine deprivation could be a promising approach for the clinical treatment of glioma.

Moreover, by elevating TP53TG1 and miR-330-3p simultaneously, we found a cell activity similar to the NC group (P > 0.05). By targeting miR-330-3p, TP53TG1 in CRC-CAF-EXs can enhance CRC cell activity and EMT capacity and inhibit apoptosis.

Methylation of the LINC00472 and SNHG6 genes can be considered as a factor in initiating ovarian cancer metastasis, and methylation of the LINC00886, MAFG-DT, and TP53TG1 genes as a colonization factor for metastases in the peritoneum. Thus, a relationship between methylation of a group of lncRNA genes at different stages of ovarian cancer dissemination was shown, which is important for understanding the mechanisms of these processes and for developing innovative approaches to ovarian cancer therapy.

Downregulation of PD-L1 increased cytokine secretion and T lymphocyte killing ability, promoted tumor cell apoptosis, and inhibited the tumor growth. Altogether, TP53TG1/STAT axis regulates the immunomodulatory mechanism of CC by reducing PD-L1 expression.

The relevance of lncRNA FAM30A with proliferation, migration ability, Daunorubicin resistance and its reciprocal action with AUF1 were demonstrated in an LSC cell line...The prognostic signature CuRS can guide prognostic stratification and personalized AML therapy. Analysis of FAM30A offers a foundation for investigating LSC-targeted therapies.

The results of qRT‒PCR further proved the accuracy of our bioinformatic analysis. Overall, our study identified a novel OSRLs signature that can serve as a promising biomarker and prognostic indicator, which provides a personalized predictive approach for patient prognosis evaluation and treatment.

In this study, identification of hypoxia regulated lncRNA with a bioinformatic pipeline consisting of a newly developed tool "GenOx" was utilized for the identification of Hypoxia Response Element (HRE) and Hypoxia Ancillary Sequence (HAS) motifs in the promoter regions of lncRNAs...Several lncRNAs have emerged as prognostic biomarkers, of which TP53TG1 and SNHG1 were identified as highly relevant lncRNAs in glioma progression and validated in hypoxia cultured cells. Significantly, we determined that SNHG1 expression in tumor (vs. normal) is different from glioma stem cells, GSC (vs. tumors) and in hypoxia (vs. normoxia), positioning downregulation of SNHG1 to be associated with worsened prognosis.