Human Pituitary Tumour Transforming Gene 1 (PTTG1) is an oncoprotein involved in maintaining chromosome stability and acts as a biomarker for a panel of cancers. In this study, we endeavoured to generate an RNA aptamer against PTTG1. The RNA aptamer, SECURA-3 has an estimated equilibrium dissociation constant of 16.41 ± 6.4 nM. The aptamer was successfully harnessed in several diagnostic platforms including ELASA, aptamer-based dot blot and aptamer-based western blot. SECURA-3 was also unveiled as a potential probe that could replace its counterpart antibody in the histostaining-based detection of PTTG1 in HeLa and MCF-7 formalin-fixed paraffin-embedded cell blocks. In the aspect of therapeutics, SECURA-3 RNA aptamer demonstrates an antagonistic effect by antagonizing the interaction between PTTG1 and CXCR2, as revealed in the in vitro competitive nitrocellulose filter binding assay and dual-luciferase reporter assay in HeLa cells. As the first anti-PTTG1 aptamer, SECURA-3 RNA aptamer has immense diagnostic and therapeutic properties.
Multiple recurrent somatic mutations have recently been identified in association with myeloproliferative neoplasms (MPN). This meta-analysis aims to assess the pooled prevalence of TET2 gene mutations among patients with MPN. Six databases (PubMed, Scopus, ScienceDirect, Google Scholar, Web of Science and Embase) were searched for relevant studies from inception till September 2020, without language restrictions. The eligibility criteria included BCR-ABL-negative MPN adults with TET2 gene mutations. A random-effects model was used to estimate the pooled prevalence with 95% confidence intervals (CIs). Subgroup analyses explored results among different continents and countries, WHO diagnostic criteria, screening methods and types of MF. Quality assessment was undertaken using the Joanna Briggs Institute critical appraisal tool. The study was registered with PROSPERO (CRD42020212223). Thirty-five studies were included (n = 5121, 47.1% female). Overall, the pooled prevalence of TET2 gene mutations in MPN patients was 15.5% (95% CI: 12.1-19.0%, I2 = 94%). Regional differences explained a substantial amount of heterogeneity. The prevalence of TET2 gene mutations among the three subtypes PV, ET and MF were 16.8%, 9.8% and 15.7%, respectively. The quality of the included studies was determined to be moderate-high among 83% of the included studies. Among patients with BCR-ABL-negative MPN, the overall prevalence of TET2 gene mutations was 15.5%.