ArticleMolecular medicine reports2021
miR‑205‑3p promotes lung cancer progression by targeting APBB2.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Advances in the biological functions of miR‑205 in various diseases (Review).Molecular medicine reports · 2026Review
- Blood-Based miRNA Panels for Timely Detection of Non-Small-Cell Lung Cancer: From Biomarker Discovery to Clinical Translation.International journal of molecular sciences · 2025Review
- Novel miRNA markers and their mechanism of esophageal squamous cell carcinoma (ESCC) based on TCGA.Scientific reports · 2024Article
- Data normalization of plasma miRNA profiling from patients with COVID-19.Scientific reports · 2024Article
- Improving CT scan for lung cancer diagnosis with an integromic signature.Journal of biological methods · 2024Article
- A comprehensive in silico analysis and experimental validation of miRNAs capable of discriminating between lung adenocarcinoma and squamous cell carcinoma.Frontiers in genetics · 2024Article
- MiR-205-3p suppresses bladder cancer progression via GLO1 mediated P38/ERK activation.BMC cancer · 2023Article
- Insights into the Mechanisms of Action of Proanthocyanidins and Anthocyanins in the Treatment of Nicotine-Induced Non-Small Cell Lung Cancer.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non‑small cell lung cancer (NSCLC), a leading cause of cancer‑associated mortality, has resulted in low survival rates and a high mortality worldwide. Accumulating evidence has suggested that microRNAs (miRs) play critical roles in the regulation of cancer progression and the present study aimed to explore the underlying mechanism of miR‑205 in NSCLC. Reverse transcription‑quantitative PCR was performed, which determined that miR‑205 expression was upregulated in NSCLC, and the present study detected the upregulation of miR‑205‑3p in a number of NSCLC cell lines and NSCLC tissues. In addition, the mediation of amyloid β precursor protein‑binding family B member 2 (APBB2) by miR‑205‑3p was demonstrated. Moreover, miR‑205‑3p was predicted to directly target the 3'untranslated region of APBB2, which was confirmed using a dual‑luciferase reporter assay. It was found that lentivirus mediated‑APBB2 knockdown could promote cellular viability and suppress apoptosis in NSCLC cells, as determined via MTT, TUNEL and flow cytometry assays. Thus, the current findings highlighted the potential promotive impact of miR‑205‑3p on NSCLC processes and may provide theoretical evidence for miR‑205‑3p as a potential clinical gene therapy target.
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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.