miR-34a suppresses proliferation and induces apoptosis of human lens epithelial cells by targeting E2F3

Xiang, Wu; Lin, Haotian; Wang, Qilin; Chen, Wan; Liu, Zhaochuan; Chen, Hui; Zhang, Hui; Chen, Weirong

doi:10.3892/mmr.2016.5901

Cited by 23 publications

(22 citation statements)

References 39 publications

(50 reference statements)

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“…24,25 Numerous studies have described the effect of miR-155 in regulating the progression of varied tumors. 26,27 There has been a trend to define miR-155 as a marker of solid and hematological malignancies for diagnosis and prognosis; 28 however, the exact role miR-155 plays in the occurrence and progression of NSCLC remains unknown. Therefore, illuminating the molecular mechanism in the occurrence and prognosis of NSCLC is of great importance.…”

Section: Discussionmentioning

confidence: 99%

MiR‐155 inhibits proliferation and invasion by directly targeting PDCD4 in non‐small cell lung cancer

Feng

Song

et al. 2017

Thoracic Cancer

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BackgroundMicroRNAs are often abnormally expressed in human non‐small cell lung cancer (NSCLC) and are thought to play a critical role in the emergence or maintenance of NSCLC by binding to its target messenger RNA. We assessed the effects of miR‐155 on cell proliferation and invasion to elucidate the role played by miR‐155/PDCD 4 in NSCLC.MethodsQuantitative reverse transcription‐PCR, Western blotting, and cell counting kit‐8, luciferase, and transwell invasion assays were conducted on a normal human bronchial epithelial cell line (BEAS‐2B) and three NSCLC cell lines (SPC‐A‐1, A549, and H2170).ResultsWe confirmed that miR‐155 was upregulated, while PDCD 4 messenger RNA and protein levels were downregulated in NSCLC cell lines. miR‐155 negatively regulated PDCD 4 at both transcriptional and post‐transcriptional levels. Moreover, PDCD 4 was forecast as an assumed target of miR‐155 using bioinformatic methods and we demonstrated that PDCD 4 was a direct target of miR‐155 using luciferase reporter assays. Furthermore, PDCD 4 overexpression could restrain NSCLC proliferation and invasion induced by miR‐155.ConclusionOur results collectively demonstrate that miR‐155 exerts an oncogenic role in NSCLC by directly targeting PDCD 4.

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Section: Discussionmentioning

confidence: 99%

MiR‐155 inhibits proliferation and invasion by directly targeting PDCD4 in non‐small cell lung cancer

Feng

Song

et al. 2017

Thoracic Cancer

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“…Recently, regulating RNAs that control gene expression has raised increasing attention in various situations. Although the role of microRNAs (miRNAs) in lenses is well established, 26 , 27 the role of lncRNAs in lens development and cataracts is still poorly understood. With previous studies reporting the existence of lncRNAs in lens development, 18 , 19 , 20 novel lncRNA ALB is the first, to our knowledge, to potentially play a role in human lens development.…”

Section: Discussionmentioning

confidence: 99%

A New Long Noncoding RNA ALB Regulates Autophagy by Enhancing the Transformation of LC3BI to LC3BII during Human Lens Development

Qin

Zhang

et al. 2017

Molecular Therapy - Nucleic Acids

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Autophagy is essential in lens organelle degradation. This study aimed to seek potential autophagy-associated long noncoding RNAs (lncRNAs) and their relative mechanisms in human lens development using the “fried egg” lentoid body (LB) generation system. The expression pattern of LC3B in differentiating LBs was similar to that in developing a mouse lens in vivo. Among the massive lncRNAs expressed with a significant difference between induced pluripotent stem cells (iPSCs) and LBs, lncRNA affecting LC3B (ALB), which was predicted to have a co-relationship with the autophagy marker LC3B, was highly expressed in differentiating lens fibers in LBs. This result was consistent with its high expression in human embryonic lenses compared to those in embryonic stem cells (ESCs). Furthermore, lncRNA ALB knockdown resulted in the downregulation of LC3BII at the protein level, therefore inhibiting the autophagy process in human lens epithelial cells (HLECs). Our results identify lncRNA ALB, a potential autophagy regulator in organelle degradation during human lens development, highlighting the importance of lncRNAs in lens development.

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“…At present, there is no effective drug to treat cataract, so we need to find targeted drugs. While miR-34a has been found to have an effect on human lens epithelial cells, making its pathogenesis in cataract an important research direction (13). In this study, the expression of miR-34a in cataract rats and its related mechanism were studied through a rat model.…”

Section: Discussionmentioning

confidence: 99%

“…SIRT1 plays an important role in the self-renewal and aging of eye stem cells and is associated with various age-related eye diseases. In human eyes, gene expression of SIRT1 in lens epithelium and retina of senile cataract patients has been detected (13,14). Studies have revealed that miR-34a can inhibit the expression of SIRT1, and SIRT1 can upregulate the expression of Nrf2 and activate the Nrf2/antioxidant response element (ES) pathway to protect cells from oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Expression of miR‑34a in cataract rats and its related mechanism

2019

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Expression of miR-34a in cataract rats and its related mechanism were investigated. A total of 30 SD rats were selected and divided into three groups: group A: 2-month-old lucent lens, group B: 18-month-old lucent lens, and group C: 18-month-old naturally occurring cataract lens. The lens was taken and measured by LOC III to determine the degree of lens opacity of the three groups of rats. qPCR was used to detect expression of miR-34a and mRNA of SIRT1 and P53. Western blotting was used to detect the protein expression of SIRT1 and P53. Cell apoptosis was detected by flow cytometry. The lens of rats in group C was more turbid than that of groups A and B (P<0.05). The expression levels of miR-34a and P53 mRNA in the rats lens of group C were significantly higher than those in groups A and B, and the expression of SIRT1 mRNA was significantly lower than that of groups A and group B (P<0.05). Expression of miR-34a in group A was significantly higher than that in group B, the mRNA expression of SIRT1 was significantly lower than that in the lucent lens of 18-month-old rats (P<0.05). The expression of SIRT1 protein in group C was significantly lower than that in groups A and group B, while the expression level of P53 protein in group C was significantly higher than that of groups A and B. The expression of SIRT1 protein in group B was significantly higher than that in group A (P<0.05). The apoptosis rate of group C was higher than that of groups A and group B (P<0.05). In conclusion, the upregulation of expression level of miR-34a is related to cataract occurrence in rats, which may be caused by regulation of SIRT1 protein.

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miR-34a suppresses proliferation and induces apoptosis of human lens epithelial cells by targeting E2F3

Cited by 23 publications

References 39 publications

MiR‐155 inhibits proliferation and invasion by directly targeting PDCD4 in non‐small cell lung cancer

MiR‐155 inhibits proliferation and invasion by directly targeting PDCD4 in non‐small cell lung cancer

A New Long Noncoding RNA ALB Regulates Autophagy by Enhancing the Transformation of LC3BI to LC3BII during Human Lens Development

Expression of miR‑34a in cataract rats and its related mechanism

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