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Long noncoding RNAs (lncRNAs) are associated with various types of cancer. However, the precise roles of many lncRNAs in tumor progression remain unclear. In this study, we found that the expression of the lncRNA TP53TG1 was downregulated in gastric cancer (GC) and it functioned as a tumor suppressor. In addition, low TP53TG1 expression was significantly associated with poor survival in patients with GC. TP53TG1 inhibited the proliferation, metastasis, and cell cycle progression of GC cells, while it promoted their apoptosis. m6A modification sites are highly abundant on TP53TG1, and demethylase ALKBH5 reduces TP53TG1 stability and downregulates its expression. TP53TG1 interacts with cancerous inhibitor of protein phosphatase 2A (CIP2A) and triggers its ubiquitination‐mediated degradation, resulting in the inhibition of the PI3K/AKT pathway. These results suggest that TP53TG1 plays an important role in inhibiting the progression of GC and provides a crucial target for GC treatment. Reveal the important role of TP53TG1 as a tumor suppressor in inhibiting the progression of gastric cancer (GC). Explore the specific mechanism by which TP53TG1 binds to CIP2A and promotes its ubiquitination, thus inhibiting the activation of the PI3K/AKT pathway. Discover the new mechanism of TP53TG1 downregulation mediated by m6A methylation modification in GC.

Long noncoding RNAs (lncRNAs) are emerging as key regulators in cancer initiation and progression. TP53TG1 is a recently identified lncRNA and several studies have shown that TP53TG1 may play the role of tumor suppressor gene or oncogene in different tumors. Nevertheless, the involvement of TP53TG1 in carcinogenesis of pancreatic ductal adenocarcinoma (PDAC) has not been characterized. In our studies, we identified that TP53TG1 was highly expressed in PDAC and was a novel regulator of PDAC development. Knockdown of TP53TG1 inhibited proliferation, induced apoptosis, and decreased migration and invasion in PDAC cells, whereas enhanced expression of TP53TG1 had the opposite effects. Mechanistically, TP53TG1 could directly bind to microRNA (miR)‐96 and effectively function as a sponge for miR‐96, thus antagonizing the functions of miR‐96 and leading to derepression of its endogenous target KRAS, which is a core oncogene in the initiation and maintenance of PDAC. Taken together, these observations imply that TP53TG1 contributes to the growth and progression of PDAC by acting as a competing endogenous RNA (ceRNA) to competitively bind to miR‐96 and regulate KRAS expression, which highlights the importance of the complicated miRNA‐lncRNA network in modulating the progression of PDAC. TP53TG1 contributes to the growth and progression of PDAC by acting as a competing endogenous RNA to upregulate KRAS expression through competitive combination with miR‐96, which highlights the importance of the complicated miRNA‐lncRNA network in modulating the progression of PDAC.

Background The acquisition of drug resistance has been considered as a main obstacle for cancer chemotherapy. Tumor protein 53 target gene 1 (TP53TG1), a p53-induced lncRNA, plays a vital role in the progression of human cancers. However, little is known about the detailed function and molecular mechanism of TP53TG1 in cisplatin resistance of NSCLC. Methods qRT-PCR analysis was used to detect the expression of TP53TG1, miR-18a and PTEN mRNA in NSCLC tissues and cells. Western blot analysis was performed to determine the protein level of PTEN and cleaved caspase-3. Cell viability and IC50 value were measured by MTT assay. Cell apoptosis was confirmed by flow cytometry assay. Subcellular fractionation assay was used to identify the subcellular location of TP53TG1. Dual-luciferase reporter assay, RNA pull down assay and RNA immunoprecipitation assay were carried out to verify the interaction between TP53TG1 and miR-18a. Xenografts in nude mice were established to verify the effect of TP53TG1 on cisplatin sensitivity of NSCLC cells in vivo. Results TP53TG1 level was downregulated in NSCLC tissues and cell lines. Upregulated TP53TG1 enhanced cisplatin sensitivity and apoptosis of A549/DDP cells, while TP53TG1 depletion inhibited cisplatin sensitivity and apoptosis of A549 cells. TP53TG1 suppressed miR-18a expression in A549 cells. Moreover, TP53TG1-mediated enhancement effect on cisplatin sensitivity was abated following the restoration of miR-18a expression in A549/DDP cells, while si-TP53TG1-induced decrease of cisplatin sensitivity and apoptosis was counteracted by miR-18a inhibitor in A549 cells. Furthermore, TP53TG1 promoted PTEN expression via inhibiting miR-18a. Finally, TP53TG1 sensitized NSCLC cells to cisplatin in vivo. Conclusion TP53TG1 increased the sensitivity of NSCLC cells to cisplatin by modulating miR-18a/PTEN axis, elucidating a novel approach to boost the effectiveness of chemotherapy for NSCLC.

Long non-coding RNA (lncRNA) TP53 target 1 (TP53TG1) is known to be strongly associated with tumor and cancer progression. However, its expression profile, unique role, and regulatory pathways in retinoblastoma (RB) are not known. Here, we revealed a large expression of TP53TG1 in RB tissues and cell lines. Conversely, we showed marked suppression of cell proliferation, migration, and invasion in TP53TG1 knocked down RB cells. Mechanistically, we established that TP53TG1 directly interacted with microRNA (miR)-33b in RB cells. Furthermore, TP53TG1 transcripts were found to be inversely correlated with miR-33b in RB tissues. We also showed that miR-33b suppression partly reversed the TP53TG1 knockdown mediated effects on tumor biology. Finally, TP53TG1 was shown to modulate the levels of SHC Binding and Spindle Associated 1 (SHCBP1), a direct target of miR-33b in RB cells. Based on the above data, we propose that TP53TG1 regulates RB progression via its modulation of the miR-33b/SHCBP1 pathway.

Tumor protein p53 target gene 1 (TP53TG1) is a significant long non-coding RNA (lncRNA) located on human chromosome 7q21.12, exhibiting dysregulated expression in several cancer tissues, and operates both as an oncogene and a tumor suppressor. TP53TG1 modulates gene expression by several mechanisms, including “competitive RNA” activity, competitive miRNA binding, control of critical signaling pathways, and facilitation of epigenetic changes. TP53TG1 affects tumor proliferation, migration, invasion, and apoptosis through intricate mechanisms, modifies tumor cells resistance to therapies, influences the tumor immune microenvironment and metabolic reprogramming, and may present various avenues for clinical therapeutic intervention. Notwithstanding considerable advancements in comprehending the molecular function of TP53TG1, some challenges persist, especially regarding the efficient and targeted administration of TP53TG1-based therapeutics. Advanced RNA delivery technologies, including lipid nanoparticles (LNPs), sphingomyelin-based nanosystems, and polymer-based nanocarriers, have demonstrated the capacity to surmount these obstacles. 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.

Long noncoding RNAs (lncRNAs) are a category of RNA molecules that exceed 200 nucleotides in length and do not possess the ability to encode proteins. Recently, there has been a growing interest among scientists regarding their functions and advancements in research. One notable lncRNA is the tumor protein 53 target gene 1 (TP53TG1), which has emerged in the last few years and is located in the chromosomal region 7q21.12 of the human genome. Studies have increasingly pointed out the role of TP53TG1 in the progression of various cancers, where its expression is altered in several tumors, including hepatocellular carcinoma, breast cancer, gastric cancer, non-small cell lung cancer, colorectal cancer, and glioma. Moreover, extensive research has shown that TP53TG1 acts as a competitive endogenous RNA (ceRNA), engaging in signaling pathways, modulating gene expression, and influencing the proliferation, migration, invasion, apoptosis, epithelial-mesenchymal transition (EMT), and drug resistance of cancer cells. Consequently, TP53TG1 is posited as a significant biomarker for tumor prognosis and is anticipated to be a potentially effective target for cancer therapies. This review article examines the expression, biological roles, and molecular mechanisms of TP53TG1 across various malignancies while exploring its clinical implications.

Long non-coding RNA (lncRNA) TP53 target 1 (TP53TG1) was discovered as a TP53 target gene. TP53TG1 has been reported as having dual roles by exerting tumor-suppressive and oncogenic activities that vary depending on the cancer type. Yet, the role of TP53TG1 in hepatocellular carcinoma (HCC) is not fully understood. In this study, we performed both gain- and loss-of-function studies to determine the biological role of TP53TG1 in HCC. We found that the knockdown of TP53 in HCC cells caused the upregulation of TP53TG1. Furthermore, we found that the knockdown of TP53TG1 not only suppressed HCC cell proliferation and migration, but also reduced intrinsic ERK signaling. In contrast, the overexpression of TP53TG1 increased ERK activation and enhanced HCC proliferation. In conclusion, our study reveals an oncogenic role of TP53TG1 in HCC, which provides a novel insight into the cell-type-specific function of TP53TG1 in HCC.

The multikinase inhibitor, sorafenib, is a first-line treatment for hepatocellular carcinoma (HCC), but its limited efficacy, drug resistance and toxicity are a concern. In this study, we investigated the role of lncRNA TP53TG1 in the efficacy of sorafenib in HCC cells. We found that treatment with sorafenib increased the expression of TP53TG1 in HCC cells. Knockdown of TP53TG1 sensitized tumor cells to the antiproliferative effects of sorafenib. Furthermore, TP53TG1 knockdown had an additive inhibitory effect on HCC cell proliferation and migration in the presence of sorafenib. The combination of TP53TG1 knockdown and sorafenib drastically inhibited the activation of the ERK pathway. This work demonstrates that TP53TG1 deficiency enhances the efficacy of sorafenib in HCC. Combining TP53TG1 knockdown with sorafenib may be an optimal form of therapy for HCC treatment.