Suppression of AKT expression by mi<scp>R</scp>‐153 produced anti‐tumor activity in lung cancer

Yuan, Ye; Du, Weijie; Wang, Ying; Xu, Chaoqian; Wang, Jinghao; Zhang, Yang; Wang, Huimin; Ju, Jiaming; Zhao, Liang; Wang, Zhiguo; Lu, Yanjie; Cai, Benzhi; Pan, Zhenwei

doi:10.1002/ijc.29103

Cited by 57 publications

(39 citation statements)

References 24 publications

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“…Knockdown of AKT expression suppressed lung cancer cell proliferation [28], and the molecules correlated with apoptosis such as Bcl-2 and caspase-3 are the downstream targets of Akt [29]. In this study, B7-H4 gene silencing induced by B7-H4 shRNA inhibited AKT phosphorylation.…”

Section: Discussionmentioning

confidence: 68%

B7-H4 promotes tumor growth and metastatic progression in lung cancer by impacting cell proliferation and survival

et al. 2017

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Aberrant expression of B7-H4 occurs across a broad spectrum of human cancers. The aim of this study was to investigate the key role of B7-H4 during tumorigenesis and metastasis of human lung cancer. Our data showed that the shRNA-mediated disruption of B7-H4 markedly inhibited tumor cell proliferation, invasion and migration, increased cell apoptosis and arrested cell cycle at G0/G1. These changes were accompanied by a marked increase in Bax and caspase-3/caspase-8, but a decrease in Bcl-2, cyclinD1 and activation of AKT. In addition, our shRNA-mediated disruption of B7-H4 led to a marked decrease in tumor growth in the immune-compromised mice. Importantly, B7-H4 was expressed in 53.33% of lung carcinomas from our patient cohort (n = 90), but not in any of adjacent non-cancerous tissues, according to our IHC analyses. In particular, B7-H4 expression appeared to be associated with lymph node metastasis (P = 0.008) and TNM stage (P = 0.012). Taken together, our study demonstrates a strong promoting role of B7-H4 in lung tumor growth, progression and metastasis, and supports its potential as a therapeutic target for the treatment of the disease.

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Section: Discussionmentioning

confidence: 68%

B7-H4 promotes tumor growth and metastatic progression in lung cancer by impacting cell proliferation and survival

et al. 2017

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“…14,15 MicroRNAs, such as miR-494, miR-153 and miR-218, inhibited lung cancer development and metastasis via suppressing cellular proliferation, inhibiting cell migration and invasion and EMT. [16][17][18] Here, we found that B3GNT3 was overexpressed in lung cancer and upregulated expression of B3GNT3 was associated with unfavorable prognosis of lung cancer patients. Silencing B3GNT3 inhibited lung cancer cell growth in vitro and suppressed lung tumor development in vivo.…”

Section: Introductionmentioning

confidence: 70%

<p>B3GNT3, a Direct Target of miR-149-5p, Promotes Lung Cancer Development and Indicates Poor Prognosis of Lung Cancer</p>

Sun¹,

Liu²,

Lu³

et al. 2020

CMAR

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These authors contributed equally to this work Background: B3GNT3 (β1, 3-N-acetylglucosaminyltransferase-3) belongs to the β3GlcNAcT family and is essential to form extended core 1 oligosaccharides. Previous studies revealed that B3GNT3 expression was dysregulated in multiple cancers. Here, we aimed to understand the expression profile and function of B3GNT3 in lung cancer. Materials and Methods: The expression of B3GNT3 was measured by immunohistochemistry and public database analysis. B3GNT3 was knocked down to evaluate the lung cancer cell proliferation, migration and invasion in in vitro and in vivo tumor formation experiments. miR-149-5p targeting B3GNT3 was identified with TargetScan analysis and confirmed with reporter assay. Overexpression of miR-149-5p was achieved using microRNA mimics and function of microRNA-149-5p/B3GNT3 axis was tested in vitro. Results: B3GNT3 was upregulated in lung cancer, and B3GNT3 overexpression was associated with poor prognosis of lung cancer patients. High expression of B3GNT3 was associated with advanced TNM stages, larger tumor size, tumor metastasis and recurrence. Functionally, we demonstrated that knockdown of B3GNT3 suppressed lung cancer cell growth and invasion in vitro. Knockdown of B3GNT3 suppressed lung cancer development in a xenograft tumor model. Moreover, miR-149-5p was validated to negatively regulate B3GNT3 expression through directly targeting B3GNT3 3ʹ-UTR. Overexpression of miR-149-5p could antagonize the tumorigenesis effect of B3GNT3 in vitro. Conclusion: In summary, our study demonstrated that B3GNT3 overexpression was correlated with poor prognosis of lung cancer patient, indicating that B3GNT3 could be a promising prognostic biomarker for lung cancer. miR-149-5p negatively regulated B3GNT3 expression, which might be utilized for therapeutic target in lung cancer.

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“…Moreover, mir‐486 was reported to be cytotoxic in A549 LUAD cells by repressing the expression of bone morphogenetic protein‐2 reporter gene . Hsa‐mir‐153 was found to be down‐regulated in NSCLC tissues and cell lines; it inhibits migration and invasion of NSCLC by targeting ADAM19 and protein kinase B ( AKT ) . These three miRNAs were speculated to serve as tumor suppressors in LUAD.…”

Section: Discussionmentioning

confidence: 99%

Identification of nine microRNAs as potential biomarkers for lung adenocarcinoma

et al. 2019

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Lung cancer is a leading global cause of cancer‐related death, and lung adenocarcinoma (LUAD) accounts for ~ 50% of lung cancer. Here, we screened for novel and specific biomarkers of LUAD by searching for differentially expressed mRNAs (DEmRNAs) and microRNAs (DEmiRNAs) in LUAD patient expression data within The Cancer Genome Atlas (TCGA). The identified optimal diagnostic miRNA biomarkers were used to establish classification models (including support vector machine, decision tree, and random forest) to distinguish between LUAD and adjacent tissues. We then predicted the targets of identified optimal diagnostic miRNA biomarkers, functionally annotated these target genes, and performed receiver operating characteristic curve analysis of the respective DEmiRNA biomarkers, their target DEmRNAs, and combinations of DEmiRNA biomarkers. We validated the expression of selected DEmiRNA biomarkers by quantitative real‐time PCR (qRT‐PCR). In all, we identified a total of 13 DEmiRNAs, 2301 DEmRNAs and 232 DEmiRNA–target DEmRNA pairs between LUAD and adjacent tissues and selected nine DEmiRNAs (hsa‐mir‐486‐1, hsa‐mir‐486‐2, hsa‐mir‐153, hsa‐mir‐210, hsa‐mir‐9‐1, hsa‐mir‐9‐2, hsa‐mir‐9‐3, hsa‐mir‐577, and hsa‐mir‐4732) as optimal LUAD‐specific biomarkers with great diagnostic value. The predicted targets of these nine DEmiRNAs were significantly enriched in transcriptional misregulation in cancer and central carbon metabolism. Our qRT‐PCR results were generally consistent with our integrated analysis. In summary, our study identified nine DEmiRNAs that may serve as potential diagnostic biomarkers of LUAD. Functional annotation of their target DEmRNAs may provide information on their roles in LUAD.

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Suppression of AKT expression by miR‐153 produced anti‐tumor activity in lung cancer

Cited by 57 publications

References 24 publications

B7-H4 promotes tumor growth and metastatic progression in lung cancer by impacting cell proliferation and survival

B7-H4 promotes tumor growth and metastatic progression in lung cancer by impacting cell proliferation and survival

<p>B3GNT3, a Direct Target of miR-149-5p, Promotes Lung Cancer Development and Indicates Poor Prognosis of Lung Cancer</p>

Identification of nine microRNAs as potential biomarkers for lung adenocarcinoma

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