MicroRNA‑133a downregulated EGFR expression in human non‑small cell lung cancer cells via AKT/ERK signaling

Guo, Ning; Zhao, Yingnan; Zhang, Wen; Li, Shaojun; Li, Shanshan; Jia, Yu

doi:10.3892/ol.2018.9399

Cited by 13 publications

(15 citation statements)

References 28 publications

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“…The over-expression of miR-133a in MCF-7 and MDA-MB-231 cells could decrease G2/S phase and interfere DNA synthesis through the EGFR/Akt signaling pathway [16]. MiRNA-133a induced NSCLC cell apoptosis and decreased cell proliferation via the EGFR/AKT/ERK signaling pathway [17]. In esophageal cancer, miR-133a could targeted EGFR, and thus promote cell apoptosis and radio-sensitivity via downregulating the MEK/ERK pathway [5].…”

Section: Mir-133a In Cell Proliferation and Apoptosismentioning

confidence: 99%

Emerging roles of MiR-133a in human cancers

Hua¹,

Xu²,

Li³

et al. 2021

J. Cancer

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MicroRNAs (miRNAs) can post-transcriptionally regulate the expression of cancer-relevant genes via binding to the 3'-untranslated region (3'-UTR) of the target mRNAs. MiR-133a, as a miRNA, participate in tumorigenesis, progression, autophagy and drug-resistance in various malignancies. Based on the recent insights, we discuss the functions of miR-133a in physiological and pathological processes and its potential effects on cancer diagnosis, prognosis and therapy.

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Section: Mir-133a In Cell Proliferation and Apoptosismentioning

confidence: 99%

Emerging roles of MiR-133a in human cancers

Hua¹,

Xu²,

Li³

et al. 2021

J. Cancer

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“…More recent studies have demonstrated that melatonin may also modulate the expression of non-coding microRNAs (or, miRNA), which modulate many aspects of tumor phenotypes in breast, liver and gastric cancers [21,22,23]. In fact, melatonin may modulate expression of specific microRNAs that function across multiple tumor types, such as miR-155, miR-133a and miR-21 [24,25,26].…”

Section: Introductionmentioning

confidence: 99%

Differential MicroRNA Expression of miR-21 and miR-155 within Oral Cancer Extracellular Vesicles in Response to Melatonin

et al. 2019

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Objective: Extracellular vesicles derived from oral cancer cells, which include Exosomes and Oncosomes, are membranous vesicles secreted into the surrounding extracellular environment. These extracellular vesicles can regulate and modulate oral squamous cell carcinoma (OSCC) progression through the horizontal transfer of bioactive molecules including proteins, lipids and microRNA (miRNA). The primary objective of this study was to examine the potential to isolate and evaluate extracellular vesicles (including exosomes) from various oral cancer cell lines and to explore potential differences in miRNA content. Methods: The OSCC cell lines SCC9, SCC25 and CAL27 were cultured in DMEM containing 10% exosome-free fetal bovine serum. Cell-culture conditioned media was collected for exosome and extracellular vesicle isolation after 72 h. Isolation was completed using the Total Exosome Isolation reagent (Invitrogen) and extracellular vesicle RNA was purified using the Total Exosome RNA isolation kit (Invitrogen). Extracellular vesicle miRNA content was evaluated using primers specific for miR-16, -21, -133a and -155. Results: Extracellular vesicles were successfully isolated from all three OSCC cell lines and total extracellular vesicle RNA was isolated. Molecular screening using primers specific for several miRNA revealed differential baseline expression among the different cell lines. The addition of melatonin significantly reduced the expression of miR-155 in all of the OSCC extracellular vesicles. However, miR-21 was significantly increased in each of the three OSCC isolates. No significant changes in miR-133a expression were observed under melatonin administration. Conclusions: Although many studies have documented changes in gene expression among various cancers under melatonin administration, few studies have evaluated these effects on microRNAs. These results may be among the first to evaluate the effects of melatonin on microRNA expression in oral cancers, which suggests the differential modulation of specific microRNAs, such as miR-21, miR-133a and miR-155, may be of significant importance when evaluating the mechanisms and pathways involved in melatonin-associated anti-tumor effects.

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“…Transmembrane‐4 L‐six family member‐1 (TM4SF1) was reported to affect cell proliferation and invasion by modulating the Akt/ERK/mTOR pathway in NSCLC . miRNA‐133a down‐regulates epidermal growth factor receptor expression in NSCLC via the AKT/ERK signaling pathway . Down‐regulation of fatty acid synthase (FASN) could markedly inhibit the expression of p‐AKT and p‐ERK in A549 cells, suggesting that FASN has an inhibitory effect on the biological functions of NSCLC cells .…”

Section: Discussionmentioning

confidence: 99%

GBX2, as a tumor promoter in lung adenocarcinoma, enhances cells viability, invasion and migration by regulating the AKT/ERK signaling pathway

Wang

Hui

et al. 2019

The Journal of Gene Medicine

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Background: Increasing evidence shows that gastrulation brain homeobox 2 (GBX2) is involved in multiple cancers. However, whether GBX2 has an effect on the lung adenocarcinoma remains unclear. In the present study, we investigated the functions of GBX2 on lung adenocarcinoma and explored the underlying mechanism.Methods: Public data were obtained from the TCGA (https://cancergenome.nih. gov) and Oncomine (http://www.oncomine.org) databases. GBX2 expression and its prognostic value were analyzed by bioinformatics methods. Relative mRNA and protein expression levels of GBX2 in lung adenocarcinoma cell lines were evaluated via a quantitative reverse transcriptase polymerase chain reaction and western blotting.Lung adenocarcinoma cell lines LTEP-a-2 and A549, respectively, were selected for gain and loss function of GBX2 assays. Cell viability was detected by CCK8 and clone formation experiments. Cell invasion and migration were assessed by Transwell assays. The effect of GBX2 on the AKT/extracellular signal regulated kinase (ERK) pathway was tested by western blotting.Results: Compared to adjacent tissues, GBX2 expression was up-regulated in lung adenocarcinoma tissues. High expression of GBX2 led to a poor survival and could be seen as an independent predictor for lung adenocarcinoma patients. Furthermore, down-regulation of GBX2 notably restrained the viability, invasion and migration abilities of A549 cells, whereas up-regulation of GBX2 in LTEP-a-2 cells presented the opposite outcomes. Furthermore, western blot indicated that down-regulation of GBX2 decreases the protein levels of phosphorylated (p)-AKT and p-ERK in A549 cells, whereas up-regulation of GBX2 shows the opposite effects in LTEP-a-2 cells. Conclusions:The results of present study indicate that GBX2 acts a cancerpromoting role to accelerate cell proliferation, invasion and migration partly by modulation of the AKT/ERK pathway in lung adenocarcinoma.

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MicroRNA‑133a downregulated EGFR expression in human non‑small cell lung cancer cells via AKT/ERK signaling

Cited by 13 publications

References 28 publications

Emerging roles of MiR-133a in human cancers

Emerging roles of MiR-133a in human cancers

Differential MicroRNA Expression of miR-21 and miR-155 within Oral Cancer Extracellular Vesicles in Response to Melatonin

GBX2, as a tumor promoter in lung adenocarcinoma, enhances cells viability, invasion and migration by regulating the AKT/ERK signaling pathway

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