New Insight into microRNA Functions in Cancer: Oncogene–microRNA–Tumor Suppressor Gene Network

Zhou, Kejun; Liu, Minxia; Cao, Yi

doi:10.3389/fmolb.2017.00046

Cited by 115 publications

(89 citation statements)

References 68 publications

(71 reference statements)

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“…microRNAs are short non‐coding RNAs demonstrated as important gene regulators (Zhou, Liu, & Cao, ). miRNAs can regulate gene expression via targeting the 3′UTRs of the target genes which can lead to either translation suppression or degradation of corresponding mRNAs (Bartel, ).…”

Section: Introductionmentioning

confidence: 99%

The lncRNA MALAT1 contributes to non‐small cell lung cancer development via modulating miR‐124/STAT3 axis

Mei

Hu³

et al. 2018

Journal Cellular Physiology

124

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lncRNAs can exert many biological effects in several cancer types. MALAT1 is a kind of lncRNA which is greatly overexpressed in several tumors including non-small cell lung cancer (NSCLC). However, the mechanism of MALAT1 in NSCLC still remains unclear. In our current study, we concentrated on the biological mechanism of MALAT1 in NSCLC. It was observed that MALAT1 was significantly upregulated in five human NSCLC cells including A549, H23, H522, H1299, and H460 cells compared to normal bronchial epithelial cell line 16HBE cells. On the contrary, miR-124 was remarkably downregulated, which indicated a potential negative correlation between miR-124 and MALAT1. MALAT1 inhibition can increase miR-124 expression in A549 and H460 cells. In addition, miR-124 mimics were able to repress MALAT1 expression and miR124 inhibitors can promote MALAT1 levels. Then it was found that shMALAT1 can inhibit NSCLC cell proliferation, colony formation and apoptosis, which can be reversed by miR-124 inhibitors. Bioinformatic analysis predicted the correlation between miR-124 and MALAT1. In addition, STAT3 was found to be a novel mRNA target of miR-124. Downregulation of MALAT1 can inhibit NSCLC development by enhancing miR-124 and decreasing STAT3 expression. We speculated that MALAT1can act as a competing endogenous lncRNA (ceRNA) to modulate miR-124/STAT3 in NSCLC. Taken these together, we revealed that MALAT1/miR-124/STAT3 was involved in NSCLC development.

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Section: Introductionmentioning

confidence: 99%

The lncRNA MALAT1 contributes to non‐small cell lung cancer development via modulating miR‐124/STAT3 axis

Mei

Hu³

et al. 2018

Journal Cellular Physiology

124

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“…Noncoding RNA includes microRNAs and LncRNAs. MicroRNAs are small ∼21‐23 nucleotides long, non‐coding RNAs which can bind to the 3′‐terminus of their target mRNAs . MicroRNA modulates a variety of cell functions, such as proliferation, apoptosis, senescence, differentiation, and cancer by controlling the expression of target genes .…”

Section: Introductionmentioning

confidence: 99%

“…MicroRNAs are small ∼21‐23 nucleotides long, non‐coding RNAs which can bind to the 3′‐terminus of their target mRNAs . MicroRNA modulates a variety of cell functions, such as proliferation, apoptosis, senescence, differentiation, and cancer by controlling the expression of target genes . Some specific miRNAs have been shown to act as tumor suppressors or as oncogenes in cancers, such as miRNA‐204‐5p to laryngeal squamous cell carcinoma progression, miRNA‐34a to prostate cancer, and miR‐22 to glioblastoma .…”

Section: Introductionmentioning

confidence: 99%

Profiling and characterization of microRNAs responding to sodium butyrate treatment in A549 cells

Xiao

Cao

Chen

2018

J of Cellular Biochemistry

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Butyrate inhibits growth of lung cancer. However, the molecular mechanism is still unclear. Here we profiled miRNAs that responded to sodium butyrate(NaB) stimulation in A549 cells, a non-small cell lung cancer cell line, using microarray. We found 33 up-regulated microRNAs and 22 down-regulated microRNAs (log2 ≥1.5 folds, P-value <0.05). The expression of miR-3935, miR-574-3p, and miR-494-3p was confirmed by realtime qPCR. Then,we explored their potential targets of miR-3935 and miR-494-3p using long noncoding RNA(LncRNA) microarray. Using cell expressing negative microRNA as control, we found 103 up-regulated transcripts (including 69 mRNA and 34 LncRNA), and 36 down-regulated transcripts (including 34 mRNAs and 2 LncRNA), in miR-3935 over-expressing A549 cells; 128 up-regulated transcripts (121 mRNAs, 7 LncRNAs) and 180 down-regulated transcripts (169 mRNAs, 11 LncRNAs) in mir-494-3p, respectively (log2 Fold change ≥ 1 & P < 0.05). The expression of RNF115, NTRK3, SLC39A6, and USB1 was confirmed with qPCR. Immunoblotting was adopted to detect RNF115 expression in miR-3935 overexpressed A549 cells. Then, using a luciferase reporter assay system, we found that miR-3935 overexpression significantly decreased 3UTR of RNF115 mediated luciferase expression .In addition, we also observed that the proliferation and migration of A549 cells was obviously prevented by miR-3935 overexpression. Finally, we showed miR-3935 and miR-494-3p induced interferon stimulated gene 15(ISG15) expression through activating its promoter transcription. Together, we profiled microRNAs that responded to NaB treatment and characterized their biological functions in A549 cells. Those results provided new clue for the future treatment of non small cell lung cancer.

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“…To date, more than 2,000 miRNAs have been verified in the human genome which may modulate the expression of approximately 30% of all the protein-coding genes (9). The deregulation of miRNA expression has been validated in almost all human cancer types and was demonstrated to be closely related with carcinogenesis and cancer progression (10)(11)(12). Numerous miRNAs are downregulated or upregulated in HCC, such as miR-21 (13), miR-493 (14), miR-873 (15) and miR-3662 (16).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑466 inhibits the aggressive behaviors of hepatocellular carcinoma by directly targeting metadherin

et al. 2018

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Numerous microRNAs (miRNAs) have been demonstrated to be downregulated or upregulated in hepatocellular carcinoma (HCC) and play important roles in its occurrence and development. Therefore, the investigation of miRNAs and their functions implicated in the genesis and development of HCC may provide key clues for the identification of effective therapeutic approaches for patients with this disease. The aims of the present study were to detect miRNA-466 (miR-466) expression in HCC tissues and cell lines and to determine its effects on HCC cell proliferation, apoptosis and metastasis, as well as to explore the mechanisms underlying the tumor-suppressing roles of miR-466 in HCC. In the present study, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to detect miR-466 expression in HCC tissues and cell lines. The effects of miR-466 upregulation on HCC cell proliferation, apoptosis, migration and invasion were determined using Cell Counting Kit-8 assay, flow cytometry analysis and Transwell chamber assay, respectively. The potential target gene of miR-466 was predicted using bioinformatic analysis, which was further confirmed by luciferase reporter assay, RT-qPCR and western blot analysis. It was found that miR-466 was obviously decreased in HCC tissues and cell lines. The results of functional experiments revealed that restoration of miR-466 expression suppressed the proliferation, induced apoptosis, and reduced the metastasis of HCC cells. In addition, metadherin (MTDH) was identified as a direct target of miR-466 in HCC cells. Furthermore, MTDH was upregulated in HCC tissues, which was inversely correlated with the miR-466 level. Moreover, inhibition of MTDH displayed similar tumor-suppressing roles as miR-466 upregulation in HCC cells. In addition, MTDH reintroduction restored the tumor-suppressor activity of miR-466 overexpression in HCC cells. These findings suggest that miR-466 is a potential therapeutic tool for HCC therapy.

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New Insight into microRNA Functions in Cancer: Oncogene–microRNA–Tumor Suppressor Gene Network

Cited by 115 publications

References 68 publications

The lncRNA MALAT1 contributes to non‐small cell lung cancer development via modulating miR‐124/STAT3 axis

The lncRNA MALAT1 contributes to non‐small cell lung cancer development via modulating miR‐124/STAT3 axis

Profiling and characterization of microRNAs responding to sodium butyrate treatment in A549 cells

MicroRNA‑466 inhibits the aggressive behaviors of hepatocellular carcinoma by directly targeting metadherin

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