biostudies-literatureUnknown10(4)Li Y<h4>Background</h4>Lung cancer is a malignant tumor with the highest morbidity and mortality rates worldwide, of which lung adenocarcinoma (LUAD) is the most common subtype. Overall, current treatments of LUAD are not satisfactory; therefore, novel targets need to be explored. Let-7b-3p is an important member of the let-7 family of microRNAs (miRNAs), and has not been studied separately in LUAD. This study aimed to investigate the role and molecular mechanism of let-7b-3p in LUAD.<h4>Methods</h4>Herein, let-7b-3p expression was detected by quantitative real-time polymerase chain reaction (qRT-PCR) and fluorescence <i>in situ</i> hybridization (FISH) assays. MTT, colony formation assay, flow cytometry analysis, wound-healing, Transwell and <i>in vivo</i> experiments were conducted to assess let-7b-3p's function in LUAD. The downstream target TFIIB-related factor 2 (BRF2) was predicted using bioinformatics analyses and confirmed by dual-luciferase reporter assay and rescue experiments. Additionally, BRF2 was found to affect the MAPK/ERK pathway through transcriptome sequencing analysis and western blot (WB) assay.<h4>Results</h4>Let-7b-3p is downregulated in LUAD cells and tissue samples and low let-7b-3p expression is correlated with a poor prognosis in LUAD patients. Let-7b-3p suppresses the proliferation and metastasis of LUAD cells both <i>in vivo</i> and <i>in vitro</i> by directly targeting the BRF2-mediated MAPK/ERK pathway.<h4>Conclusions</h4>Let-7b-3p inhibits the development of LUAD and is an ideal novel therapeutic target for the treatment of LUAD.Translational lung cancer research1841-1856https://www.ebi.ac.uk/biostudies/studies/S-EPMC8107730biostudies-literatureLet-7b-3p inhibits tumor growth and metastasis by targeting the BRF2-mediated MAPK/ERK pathway in human lung adenocarcinoma.PMC8107730Cheng CRenaud SJiang JLi YLu MFeng ZZhao RTian HLiang JHan JXu-Welliver MDong RfalseLet-7b-3p inhibits tumor growth and metastasis by targeting the BRF2-mediated MAPK/ERK pathway in human lung adenocarcinoma.<h4>Background</h4>Lung cancer is a malignant tumor with the highest morbidity and mortality rates worldwide, of which lung adenocarcinoma (LUAD) is the most common subtype. Overall, current treatments of LUAD are not satisfactory; therefore, novel targets need to be explored. Let-7b-3p is an important member of the let-7 family of microRNAs (miRNAs), and has not been studied separately in LUAD. This study aimed to investigate the role and molecular mechanism of let-7b-3p in LUAD.<h4>Methods</h4>Herein, let-7b-3p expression was detected by quantitative real-time polymerase chain reaction (qRT-PCR) and fluorescence <i>in situ</i> hybridization (FISH) assays. MTT, colony formation assay, flow cytometry analysis, wound-healing, Transwell and <i>in vivo</i> experiments were conducted to assess let-7b-3p's function in LUAD. The downstream target TFIIB-related factor 2 (BRF2) was predicted using bioinformatics analyses and confirmed by dual-luciferase reporter assay and rescue experiments. Additionally, BRF2 was found to affect the MAPK/ERK pathway through transcriptome sequencing analysis and western blot (WB) assay.<h4>Results</h4>Let-7b-3p is downregulated in LUAD cells and tissue samples and low let-7b-3p expression is correlated with a poor prognosis in LUAD patients. Let-7b-3p suppresses the proliferation and metastasis of LUAD cells both <i>in vivo</i> and <i>in vitro</i> by directly targeting the BRF2-mediated MAPK/ERK pathway.<h4>Conclusions</h4>Let-7b-3p inhibits the development of LUAD and is an ideal novel therapeutic target for the treatment of LUAD.2021-01-01T00:00:00Z2021 Apr2025-04-27T00:16:47.402Z2025-04-06T17:46:44.563ZS-EPMC81077303401279710.21037/tlcr-21-299