ArticleScientific reports2020
lncRNA AFAP1-AS1 promotes triple negative breast cancer cell proliferation and invasion via targeting miR-145 to regulate MTH1 expression.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.
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Who cites it
27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 52 citations in OpenAlex.
- Roles of AFAP1-AS1 in Gynecology and Urogenital System.Current pharmaceutical design · 2024Pooled it
- Prognostic value of lncRNA AFAP1-AS1 in breast cancer: a meta-analysis and validated study in Chinese population.Cancer reports (Hoboken, N.J.) · 2024Pooled it
- The interplay of the lncRNA AFAP1-AS1 and the soluble immune checkpoint proteins sPD-1/sPD-L1 in breast cancer: tumor-immune cross-talk.Bioscience reports · 2026Article
- Antisense oligonucleotides: targeting oncogenic long non-coding RNAs for cancer therapy.Biotechnology letters · 2026Review
- Potential role ofBiochemistry and biophysics reports · 2026Article
- Repurposing resveratrol for redox-mediated inhibition of MTH1 in breast cancer.Scientific reports · 2025Article
- Role of MTH1 in oxidative stress and therapeutic targeting of cancer.Redox biology · 2024Review
- Targeting the nucleic acid oxidative damage repair enzyme MTH1: a promising therapeutic option.Frontiers in cell and developmental biology · 2024Review
- Omics-driven investigation of the biology underlying intrinsic submaximal working capacity and its trainability.Physiological genomics · 2023Article
- SP1-Induced Upregulation of LncRNA AFAP1-AS1 Promotes Tumor Progression in Triple-Negative Breast Cancer by Regulating mTOR Pathway.International journal of molecular sciences · 2023Article
- Construction of a predictive model for breast cancer metastasis based on lncRNAs.Translational cancer research · 2023Article
- Long Non Coding RNA in Triple Negative Breast Cancer: A Promising Biomarker in Tumorigenesis.Asian Pacific journal of cancer prevention : APJCP · 2023Review
- CTCF-Induced lncRNA C5orf66-AS1 Facilitates the Progression of Triple-Negative Breast Cancer via Sponging miR-149-5p to Up-Regulate CTCF and CTNNB1 to Activate Wnt/β-Catenin Pathway.Molecular and cellular biology · 2022Article
- Article
- The Curcumin Analog EF24 Inhibits Proliferation and Invasion of Triple-Negative Breast Cancer Cells by Targeting the Long Noncoding RNA HCG11/Sp1 Axis.Molecular and cellular biology · 2022Article
- Circulating non-coding RNAs as a diagnostic and management biomarker for breast cancer: current insights.Molecular biology reports · 2022Review
- Advances in Pathophysiology of Triple-Negative Breast Cancer: The Potential of lncRNAs for Clinical Diagnosis, Treatment, and Prognostic Monitoring.Molecular biotechnology · 2021Review
- Article
- Long noncoding RNA AFAP1-AS1 promotes tumor progression and invasion by regulating the miR-2110/Sp1 axis in triple-negative breast cancer.Cell death & disease · 2021Article
- Circ_0082182 promotes oncogenesis and metastasis of colorectal cancer in vitro and in vivo by sponging miR-411 and miR-1205 to activate the Wnt/β-catenin pathway.World journal of surgical oncology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The actin fiber-associated protein 1-antisense RNA1 (AFAP1-AS1) is upregulated in various cancers and associated with cancer proliferation and metastasis. Several cancer-related pathways have been linked to up-expression of this long non-coding (lnc)RNA, but the underlying mechanisms are yet unknown. In triple negative breast cancer (TNBC), AFAP1-AS1 expression is also significantly overexpressed compared to that in other subtypes of breast cancer from the TCGA dataset. In this study, we performed bioinformatic RNAhybrid analyses and identified that miR-145 is a potential target of AFAP1-AS1 and able to reduce MutT homolog-1 (MTH1) expression. Thus, this study investigated the oncogenic activity of AFAP1-AS1 in TNBC cells and the underlying mechanisms that are yet poorly understood. The results showed that miR-145 expression was low, whereas AFAP1-AS1 and MTH1 expression was high in TNBC cells and that miR-145 mimics reduced TNBC cell proliferation and invasion, whereas miR-145 knockdown exerted the opposite activity in TNBC cells. Moreover, knockdown of AFAP1-AS1 reduced tumor cell proliferation and invasion, but miR-145 co-transfection rescued tumor cell viability and colony formation ability. The dual luciferase reporter assay showed that AFAP1-AS1 could directly target miR-145, while miR-145 could directly target MTH1. After knockdown of ATF6, AFAP1-AS1 was reduced along with AFAP1-AS1 promoter activity. This study revealed that AFAP1-AS1 could promote TNBC cell proliferation and invasion via regulation of MTH1 expression through targeting of miR-145.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.