microRNA‐148a‐3p inhibited the proliferation and epithelial–mesenchymal transition progression of non‐small‐cell lung cancer via modulating Ras/MAPK/Erk signaling

Qiong, Xie; Yu, Zipu; Lu, Yuan; Fan, Jingya; Ni, Yiming; Ma, Liang

doi:10.1002/jcp.27899

Cited by 55 publications

(45 citation statements)

References 21 publications

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“…A detailed investigation of cancer-associated miRNAs in NScLc is therefore crucial for identifying effective therapeutic targets for this disease. Previous studies have focused on miRNAs expression profiles and functions during the development of NScLc (36)(37)(38); however, the association between miR-625 and NScLc requires further investigation. To the best of our knowledge, the present study is the first to assess miR-625 expression in NScLc and investigated its clinical value in patients with NSCLC.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-625 inhibits the progression of non‑small cell lung cancer by directly targeting HOXB5 and deactivating the Wnt/β-catenin pathway

Tan

Jiang

et al. 2019

Int J Mol Med

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Numerous microRNAs (miRs) are dysregulated in non-small cell lung cancer (NScLc), serving pivotal roles in its formation and progression. miR-625 is dysregulated in several types of human cancer, but its involvement in the formation and development of NScLc remains poorly understood. In the present study, we aimed to investigate miR-625 expression in NScLc and its role in regulating NScLc cell behavior. miR-625 expression in NScLc tissues and cell lines was detected using reverse transcription-quantitative polymerase chain reaction. The effects of miR-625 overexpression on NScLc cell proliferation, apoptosis, migration and invasion in vitro were assessed using an MTT assay, flow cytometry, and cell migration and invasion assays, respectively. The effects of miR-625 upregulation on NScLc growth were evaluated in an in vivo xenograft model. The molecular mechanisms underlying the tumor-suppressing roles of miR-625 in NScLc were explored in detail. miR-625 expression was determined to be downregulated in NScLc tissues and cell lines. This decreased expression was associated with advanced clinical features and poor overall survival of patients with NScLc. Exogenous miR-625 expression suppressed NScLc cell proliferation, migration and invasion, and induced apoptosis in vitro. miR-625 upregulation hindered NScLc tumor growth in vivo. Homeobox B5 (HOXB5) was proposed to be the direct target gene of miR-625 in NScLc cells. The tumor-suppressing effects of HOXB5 silencing were similar to those of miR-625 overexpression in NScLc cells. In rescue experiments, HOXB5 overexpression partially reversed the inhibitory effects of miR-625 in NScLc cells. miR-625 upregulation directly targeted HOXB5 to deactivate the Wnt/β-catenin signaling pathway in NScLc cells in vitro and in vivo. miR-625 was determined to be associated with HOXB5 suppression and Wnt/β-catenin pathway deactivation, which in turn inhibited the aggressive behavior of NScLc cells in vitro and in vivo.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-625 inhibits the progression of non‑small cell lung cancer by directly targeting HOXB5 and deactivating the Wnt/β-catenin pathway

Tan

Jiang

et al. 2019

Int J Mol Med

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“…Seviour and co-workers reported that miR-193a-3p directly targets KRAS and inhibits KRAS-mutated lung tumor growth in vivo [30], while miR-181a-5p was also observed to inhibit the proliferation and migration of A549 cells through downregulating KRAS [31]. Additionally, miR-148a-3p was shown to inhibit NSCLC cell proliferation in vitro via the suppression of SOS2, a molecule upstream of the Ras signaling pathway [32]. Jiang et al also reported that miR-1258 might target GRB2 and inhibit Grb2, the upstream protein required for downstream Ras activation, which further downregulates the MEK/ERK pathway in mice models [33].…”

Section: The Role Of Mirna In Lung Cancer Development and Behaviormentioning

confidence: 99%

The Roles of MicroRNA in Lung Cancer

Tsai

Lien

et al. 2019

IJMS

214

175

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Lung cancer is the most devastating malignancy in the world. Beyond genetic research, epigenomic studies—especially investigations of microRNAs—have grown rapidly in quantity and quality in the past decade. This has enriched our understanding about basic cancer biology and lit up the opportunities for potential therapeutic development. In this review, we summarize the involvement of microRNAs in lung cancer carcinogenesis and behavior, by illustrating the relationship to each cancer hallmark capability, and in addition, we briefly describe the clinical applications of microRNAs in lung cancer diagnosis and prognosis. Finally, we discuss the potential therapeutic use of microRNAs in lung cancer.

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“…The crosstalk between the two pathways perhaps demonstrates how multiple pathways become involved in tumorigenesis and proliferation, and by targeting one can reduce activation of the other. Xie and colleagues looked at miR-148a-3p, a tumor growth suppressor found in NSCLC, and found that it had a role in MAPK/ERK inhibition via overexpression which led to decreased presence of son of sevenless homolog 2 (SOS2) and consequently inhibited Ras activation [203]. Alternatively, targeting activated KRAS with overexpression of tumor suppressors miR-193a-3p [204,205] and miR-181a-5p [206,254] could potentially inhibit further progression of tumor growth.…”

Section: Ras/raf/mek/erk (Mapk)mentioning

confidence: 99%

Non-Coding RNAs in Lung Tumor Initiation and Progression

Santos

Moreno

Zhang

2020

IJMS

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Lung cancer is one of the deadliest forms of cancer affecting society today. Non-coding RNAs, such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), through the transcriptional, post-transcriptional, and epigenetic changes they impose, have been found to be dysregulated to affect lung cancer tumorigenesis and metastasis. This review will briefly summarize hallmarks involved in lung cancer initiation and progression. For initiation, these hallmarks include tumor initiating cells, immortalization, activation of oncogenes and inactivation of tumor suppressors. Hallmarks involved in lung cancer progression include metastasis and drug tolerance and resistance. The targeting of these hallmarks with non-coding RNAs can affect vital metabolic and cell signaling pathways, which as a result can potentially have a role in cancerous and pathological processes. By further understanding non-coding RNAs, researchers can work towards diagnoses and treatments to improve early detection and clinical response.

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microRNA‐148a‐3p inhibited the proliferation and epithelial–mesenchymal transition progression of non‐small‐cell lung cancer via modulating Ras/MAPK/Erk signaling

Cited by 55 publications

References 21 publications

MicroRNA-625 inhibits the progression of non‑small cell lung cancer by directly targeting HOXB5 and deactivating the Wnt/β-catenin pathway

MicroRNA-625 inhibits the progression of non‑small cell lung cancer by directly targeting HOXB5 and deactivating the Wnt/β-catenin pathway

The Roles of MicroRNA in Lung Cancer

Non-Coding RNAs in Lung Tumor Initiation and Progression

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