Effect and molecular mechanism of mir-146a on proliferation of lung cancer cells by targeting and regulating MIF gene

Wang, Wuming; Liu, Jichun

doi:10.1016/j.apjtm.2016.06.001

Cited by 15 publications

(12 citation statements)

References 29 publications

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“…This might arise from the inhibition of cell proliferation, differentiation, and migration by miR-146a through regulating several pathways. [ 20 , 23 ] In addition, we also found that high expressions of tissue miR-146a and plasma miR-146a were associated with better OS, whereas only tissue miR-146a high expression was an independent factor for prolonged OS of ICC patients. There are 2 possible reasons.…”

Section: Discussionmentioning

confidence: 59%

“…Upregulation of miR-146a inhibits lung cancer cell proliferation and differentiation via mediating the macrophage migration inhibitory factor (MIF) gene and NF-κB signaling pathway. [ 20 ] Also, its overexpression represses gastric cancer cell migration by reducing the UHRF1 level via targeting its 3′-UTR, resulting in the inhibition of tumor invasion and metastasis subsequently. [ 21 ] Additionally, miR-146a expression has been observed to be positively associated with antitumor immune systems by targeting signal transducer and activator of transcription 3 (STAT3) in human hepatocellular carcinoma (HCC) cells.…”

Section: Discussionmentioning

confidence: 99%

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Both plasma and tumor tissue miR-146a high expression correlates with prolonged overall survival of surgical patients with intrahepatic cholangiocarcinoma

Zhang

Zheng²,

Li³

et al. 2017

Medicine

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The purpose of this study was to investigate the association of tumor tissue and plasma miR-146a/b expressions with the clinicopathological properties and overall survival (OS) in surgical patients with intrahepatic cholangiocarcinomas (ICC).Eighty-seven patients with ICC were enrolled. Tumor tissue and plasma sample were collected and miR-146a/b expressions were assessed by quantitative polymerase chain reaction (qPCR). The median follow-up duration was 31 months, and the last follow-up date was January 2017.miR-146a (P < .001) and miR-146b (P = .006) expressions in tumor tissue were positively associated with that in plasma. Tissue miR-146a was negatively correlated with age (P = .036), poor differentiation (P = .020), N stage (P = .020), and TNM stage (P = .007), as well as ECOG performance (P = .008), whereas plasma miR-146a was inversely associated with N stage (P = .003), TNM stage (P = .003), and ECOG performance (P = .011). Moreover, tissue miR-146b was negatively correlated with gender (P = .043) and T stage (P = .047). Kaplan-Meier curves suggested that high expression of tissue miR-146a (P < .001) and plasma miR-146a (P = .029) were correlated with prolonged OS. Nevertheless, no association of miR-146b expression in tumor tissue (P = .187) and plasma (P = .336) with OS was discovered. Univariate analysis indicated that both tissue miR-146a (P < .001) and plasma miR-146a (P = .035) could predict better OS, whereas multivariate analysis revealed that only tissue miR-146a (P = .001) high expression was an independent factor for prolonged OS.Both plasma and tissue miR-146a expression correlated with favorable OS, whereas only tissue miR-146a was an independent prognostic biomarker in surgical patients with ICC.

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Both plasma and tumor tissue miR-146a high expression correlates with prolonged overall survival of surgical patients with intrahepatic cholangiocarcinoma

Zhang

Zheng²,

Li³

et al. 2017

Medicine

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“…miRNAs are involved in the regulation of diverse biological processes, including invasion, migration, proliferation and cell apoptosis ( 14 – 16 ). Abnormal expression of miRNAs, including the upregulation of miR-429 ( 17 ), miR-19a ( 18 ) and miR-146a ( 19 ), and downregulation of miR-143 ( 20 ), miR-3666 ( 21 ) and miR-29b ( 22 ) have been detected in lung cancer. Thus, miRNAs have potential as biomarker for diagnosis, targeted therapy and prognosis.…”

Section: Introductionmentioning

confidence: 99%

miR-25 enhances cell migration and invasion in non-small-cell lung cancer cells via ERK signaling pathway by inhibiting KLF4

et al. 2018

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In recent years, microRNAs (miRNAs/miRs) have gained increasing interest in cancer research. Increasing evidences demonstrated that miRNAs are important for tumor early detection and prognosis. The present study aimed to explore the function of miR-25 in non-small-cell lung cancer (NSCLC) and its underlying mechanisms. The expression levels of miR-25 and Krüppel-like factor 4 (KLF4) were assessed in 31 pairs of tissue from patients with NSCLC. In addition, the biological roles of miR-25 in NSCLC were analyzed via a cell wound healing assay, Transwell invasion and migration assays. Target genes of miR-25 were predicted using TargetScan and verified via a dual luciferase activity assay, western blotting and reverse transcription-quantitative polymerase chain reaction. The downstream signaling pathway was confirmed by western blot analysis. In the present study, miR-25 was overexpressed in 31 NSCLC samples compared with in corresponding normal tissues. Overexpression of miR-25 using miR-25 mimics markedly promoted NSCLC cell migration and invasion, while inhibition of miR-25 exerted the opposite effect. KLF4 was suggested to be a novel target gene of miR-25 in NSCLC cells. Knockdown of KLF4 promoted the migration and invasion of NSCLC cells, whereas rescue of KLF4 expression reduced cell motion ability in miR-25-overexpressing NSCLC cells. Furthermore, it was demonstrated that miR-25 activated the extracellular signal-regulated kinase (ERK) signaling pathway, which eventually led to increased vimentin, matrix metalloproteinase 11 and N-cadherin levels, and the downregulation of E-cadherin expression by inhibiting the expression of KLF4. In conclusion, miR-25 was demonstrated to activate the ERK signaling pathway by directly targeting KLF4, promoting cell migration and invasion. The findings of the present study indicated that miR-25 or KLF4 may serve as a therapeutic target for the treatment of NSCLC.

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“…However, in 2013, Chen et al (37) reported that the expression of miR-146a was reduced in NSCLC, which suggested that miR-146a may have a role as a tumor suppressor gene. Wang et al (38) showed similar results. These data indicated that, in lung cancer, the role of miR-146a and whether it acts as an oncogene or a tumor suppressor gene remains debatable.…”

Section: Discussionmentioning

confidence: 62%

Effect and mechanism of miR‑146a on malignant biological behaviors of lung adenocarcinoma cell line

et al. 2020

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The aim of the present study was to assess the expression of microRNA-146a (miR-146a) in human lung adenocarcinoma cells, its effect on cellular behaviors, and the underlying molecular mechanisms. Reverse transcription-quantitative PCR (RT-qPCR) was used to measure miR-146a expression in the human normal lung epithelial cell line, BEAS-2B, and human lung adenocarcinoma cell lines, A549, PC-9 and H1299, to determine whether miR-146a acts as an oncogene or anti-oncogene. miR-146a mimics were transfected into target cells to observe the proliferation, apoptosis, invasion and migration of human lung adenocarcinoma cells. The target genes of miR-146a were predicted using bioinformatics analysis, and binding sites were validated by dual-luciferase reporter assay. Target gene expression at the mRNA and protein levels was measured by RT-qPCR and western blot analysis, respectively. The expression levels of miR-146a in human lung adenocarcinoma cell lines were lower than its expression in BEAS-2B (P<0.01). A549 cell line is a EGFR wild-type lung adenocarcinoma cell line, which is also the most widely studied in NSCLC, and therefore this was chosen as the target cell line for further investigation. Overexpression of miR-146a in A549 cells can inhibit cell proliferation (P<0.05), promote apoptosis (P<0.05), and reduce the cells' migratory ability (P<0.01). Bioinformatics prediction indicated that interleukin-1 receptor-associated kinase 1 (IRAK1) and TNF receptor associated factor 6 (TRAF6) are the target genes of miR-146a. Dual-luciferase reporter assay showed that miR-146a could specifically bind to 3'-untranslated regions of IRAK1 and TRAF6. The protein and mRNA levels of IRAK1 and TRAF6 were significantly downregulated after miR-146a overexpression in A549 cells (P<0.01). The results of this study demonstrated that the expression of miR-146a in human lung adenocarcinoma cells was significantly lower than in normal lung epithelial cells, indicating that miR-146a acts as an anti-oncogene. miR-146a suppresses the proliferation and migration of human lung adenocarcinoma cells by downregulating the expression of IRAK1 and TRAF6.

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Effect and molecular mechanism of mir-146a on proliferation of lung cancer cells by targeting and regulating MIF gene

Cited by 15 publications

References 29 publications

Both plasma and tumor tissue miR-146a high expression correlates with prolonged overall survival of surgical patients with intrahepatic cholangiocarcinoma

Both plasma and tumor tissue miR-146a high expression correlates with prolonged overall survival of surgical patients with intrahepatic cholangiocarcinoma

miR-25 enhances cell migration and invasion in non-small-cell lung cancer cells via ERK signaling pathway by inhibiting KLF4

Effect and mechanism of miR‑146a on malignant biological behaviors of lung adenocarcinoma cell line

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