MicroRNA-124 suppresses proliferation and glycolysis in non–small cell lung cancer cells by targeting AKT–GLUT1/HKII

Zhao, Xiaojie; Lu, Caiping; Chu, Weiwei; Zhang, Bing; Zhen, Qiang; Wang, Renfeng; Zhang, Yaxiao; Li, Zhe; Lv, Baolei; Li, Huixian; Liu, Jia‐Bao

doi:10.1177/1010428317706215

Cited by 81 publications

(60 citation statements)

References 23 publications

(29 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Specifically, downregulated miR-124 expression was identified in several types of cancer,16, 17, 18 and studies have shown that the overexpression of miR-124 suppresses cancer progression by inhibiting the Akt pathway,14, 17 which suggests that miR-124 may play a general role in the regulation of the Akt pathway in different types of cancer. The downregulated expression of miR-124 in lung cancer tissues 19 and the negative correlation between miR-124 and p-Akt in lung cancer cells 20 have been previously reported. However, the detailed mechanism by which miR-124 regulates Akt phosphorylation is not clear in NSCLC cells.…”

Section: Introductionsupporting

confidence: 52%

miR-124 Inhibits Lung Tumorigenesis Induced by K-ras Mutation and NNK

Jin

Cao

et al. 2017

Molecular Therapy - Nucleic Acids

View full text Add to dashboard Cite

Dysregulated miRNAs play important role in K-ras mutation or smoking caused lung tumorigenesis. Here, we investigate the role and mechanism of miR-124 in K-ras mutation or smoking-caused lung tumorigenesis and evaluate the therapeutic potential of miR-124 agomiR in K-ras mutation or smoking-caused lung cancer treatment. Our data show that smoking suppresses miR-124 expression, and decreased miR-124 expression is inversely correlated with the p-Akt level and predicts poor overall survival in non-small-cell lung cancer (NSCLC) patients. The overexpression of miR-124 suppressed NSCLC growth by inhibiting the Akt pathway by targeting Akt1 and Akt2. In addition, the systemic delivery of miR-124 agomiR dramatically suppressed tumorigenesis in both NNK-induced lung cancer model and K-rasLA1 transgenic mice by increasing apoptosis and inhibiting cell proliferation. Our findings suggest that smoking inhibits the expression of miR-124, and decreased miR-124 contributes to Akt activation, thereby promoting NSCLC progression. Our findings also represent a novel potential therapeutic strategy for lung cancer.

show abstract

Section: Introductionsupporting

confidence: 52%

miR-124 Inhibits Lung Tumorigenesis Induced by K-ras Mutation and NNK

Jin

Cao

et al. 2017

Molecular Therapy - Nucleic Acids

View full text Add to dashboard Cite

show abstract

“…MiRNAs have been associated with the initiation and progression of NSCLC (31)(32)(33). As such, a comprehensive understanding of the association between dysregulated miRNA expression and NSCLC may contribute to the identification of novel therapeutic methods for patients with this disease.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑433 reduces cell proliferation and invasion in non‑small cell lung cancer via directly targeting E2F transcription factor 3

Liu

Zhang

et al. 2018

Mol Med Report

View full text Add to dashboard Cite

MicroRNAs (miRNA/miRs) have been associated with the initiation and progression of non‑small‑cell lung cancer (NSCLC). Hence, a comprehensive understanding of the association between dysregulated miRNAs and NSCLC may contribute to the identification of novel therapeutic methods for patients with NSCLC. MiRNA‑433 (miR‑433) has been reported to be dysregulated in numerous types of human cancers; however, its expression pattern, biological roles and associated mechanisms in NSCLC require further investigation. The present study aimed to detect miR‑433 expression and determine its roles and underlying molecular mechanisms in NSCLC. In the present study, reverse transcription‑quantitative polymerase chain reaction revealed that miR‑433 was significantly downregulated in NSCLC tissues and cell lines. This decreased miR‑433 expression was strongly associated with the tumor node metastasis stage and lymph node metastasis of patients with NSCLC. Cell Counting kit‑8 and cell invasion assays revealed that the resumption of miR‑433 expression decreased the proliferation and invasion of NSCLC cells. Bioinformatics analysis predicted E2F transcription factor 3 (E2F3) as a potential target of miR‑433. Luciferase reporter assay, RT‑qPCR and western blot analysis further demonstrated that E2F3 was a direct target of miR‑433 in NSCLC. E2F3 downregulation induced by small interfering RNA exhibited inhibitory effects similar to those of miR‑433 overexpression in NSCLC cells, and the restored E2F3 expression counteracted the suppressive effects on NSCLC cells induced by miR‑433 overexpression. Therefore, miR‑433 may inhibit the progression of NSCLC, at least in part, by targeting E2F3. The present study indicated that miR‑433 may be investigated as an innovative candidate target for the therapy of patients with this fatal disease.

show abstract

“…MicroRNAs (miRNAs/miRs) are a class of small RNAs that serve essential functions in various physiological and pathological processes (3)(4)(5). A large body of evidence has demonstrated that the dysregulation of miRNA expression has been identified in a number of different types of cancer (6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

Targeting of TLE3 by miR‑3677 in human breast cancer promotes cell proliferation, migration and invasion

et al. 2019

View full text Add to dashboard Cite

Numerous studies have indicated an important function of microRNAs (miRs) in breast cancer (BC) progression, oncogenesis and metastasis. However, the function of miR-3677, which has been revealed to be upregulated in BC [The Cancer Genome Atlas (TCGA) data], has not been investigated to date. In the present study, miR-3677 was revealed to be upregulated in BC as determined using TCGA. miR-3677 was significantly upregulated in BC tissues and cell lines compared with those noted in adjacent non-cancerous tissues and primary normal breast cells (P<0.05). The overexpression of miR-3677 promoted the cell proliferation, migration and invasion of BC cells. Using bioinformatics algorithms and luciferase assays, a novel target gene for miR-3677, namely transducin-like enhancer of Split3 (TLE3), was identified. Silencing of TLE3 in miR-3677-transfected BC cells suppressed their proliferation and migration. An inverse correlation was observed between miR-3677 and TLE3 expression levels in human BC tissues. In conclusion, the present study demonstrated that miR-3677 promoted BC cell proliferation, migration and invasion by inhibiting TLE3 expression, which provided a novel mechanism and a promising therapeutic target for patients with BC.

show abstract

MicroRNA-124 suppresses proliferation and glycolysis in non–small cell lung cancer cells by targeting AKT–GLUT1/HKII

Cited by 81 publications

References 23 publications

miR-124 Inhibits Lung Tumorigenesis Induced by K-ras Mutation and NNK

miR-124 Inhibits Lung Tumorigenesis Induced by K-ras Mutation and NNK

MicroRNA‑433 reduces cell proliferation and invasion in non‑small cell lung cancer via directly targeting E2F transcription factor 3

Targeting of TLE3 by miR‑3677 in human breast cancer promotes cell proliferation, migration and invasion

Contact Info

Product

Resources

About