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Objective: Lung squamous cell carcinoma is typically associated with a poor prognosis, highlighting the need for a reliable prognostic marker. Given that the long noncoding RNA TPT1-AS1 has demonstrated aberrant expression in numerous cancers, the prognostic significance of TPT1-AS1 in LUSC was examined. Methods: The present study included 115 patients diagnosed with LUSC. The expression levels of TPT1-AS1 and miR-4726-5p in tissues and cells were assessed using RT-qPCR, while the correlation between TPT1-AS1 expression and clinicopathological features was analyzed through the chi-square test. Binding sites between TPT1-AS1 and miR-4726-5p were predicted using a database and confirmed via a dual-luciferase reporter assay. The Pearson correlation coefficients were calculated to determine the relationship between TPT1-AS1 and miR-4726-5p in tumor tissues. The impacts of TPT1-AS1 and miR-4726-5p on cells were evaluated through CCK-8 and Transwell assays. Results: TPT1-AS1 expression was found to be reduced, while miR-4726-5p expression was upregulated in LUSC tissues. Patients exhibiting low TPT1-AS1 expression experienced shorter overall survival. Moreover, TPT1-AS1 was identified as an independent prognostic factor. A dual luciferase reporter assay validated that TPT1-AS1-WT targeted and bound to miR-4726-5p. Additionally, an inverse correlation was observed between miR-4726-5p and TPT1-AS1 in tumors. Cell experiments indicated that the overexpression of TPT1-AS1 led to a decrease in miR-4726-5p expression, consequently inhibiting cell proliferation, migration, and invasion. Conclusion: TPT1-AS1 targets miR-4726-5p, and overexpression of TPT1-AS1 has the potential to serve as a prognostic marker for LUSC and can significantly influence LUSC progression. [ABSTRACT FROM AUTHOR]

Human diseases are multifactorial processes mainly driven by the intricate interactions of genetic and environmental factors. Long noncoding RNAs (lncRNAs) represent a type of non-coding RNAs with more than 200 nucleotides. Multiple studies have demonstrated that the dysregulation of lncRNAs is associated with complex biological as well as pathological processes through various mechanism, especially the regulation of gene transcription and related signal transduction pathways. Moreover, an increasing number of studies have explored lncRNA-based clinical applications in different diseases. For instance, the lncRNA Tumor Protein Translationally Controlled 1 (TPT1) Antisense RNA 1 (TPT1-AS1) was found to be dysregulated in several types of disease and strongly associated with patient prognosis and diverse clinical features. Recent studies have also documented that TPT1-AS1 modulates numerous biological processes through multiple mechanisms, including cell proliferation, apoptosis, autophagy, invasion, migration, radiosensitivity, chemosensitivity, stemness, and extracellular matrix (ECM) synthesis. Furthermore, TPT1-AS1 was regarded as a promising biomarker for the diagnosis, prognosis and treatment of several human diseases. In this review, we summarize the role of TPT1-AS1 in human diseases with the aspects of its expression, relevant clinical characteristics, molecular mechanisms, biological functions, and subsequent clinical applications. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) are key modulators during cancer progression. Application of using lncRNA expression to evaluate patient prognosis and sensitivity to treatment is highly anticipated, yet the expression and mechanism of many lncRNAs remain unknown. Herein, we projected for the investigation of TPT1-AS1 function in breast cancer. TPT1-AS1 was assessed by bioinformatic analysis of publicly available datasets and quantitative real-time PCR (qRT-PCR). Cell sensitivity to paclitaxel and cell proliferation was measured by flow cytometry and CCK-8. Interaction among TPT1-AS1, microRNA (miRNA, miR)-3156-5p and Caspase 2 (CASP2) was studied by bioinformatic analysis, qRT-PCR, western blot as well as dual luciferase reporter assay. Herein, TPT1-AS1 was significantly diminished in breast cancer from publicly available datasets and our collected samples. In breast cancer cells, TPT1-AS1 overexpression repressed cell proliferation and sensitized breast cancer cells to paclitaxel. RegRNA 2.0 predicted a potential interaction between TPT1-AS1 and miR-3156-5p which was confirmed by qRT-PCR as well as dual luciferase reporter assay. CASP2, a proapoptotic gene, was corroborated to be targeted by miR-3156-5p. Meanwhile, TPT1-AS1 upregulated CASP2 in breast cancer cells, and its biological function was reversed by CASP2 knockdown. Collectively, TPT1-AS1 diminished cell proliferation and sensitized cells to chemotherapy by sponging miR-3156-5p and upregulating CASP2, acting as a biomarker for patients with breast cancer. [ABSTRACT FROM AUTHOR]