microRNA-137 functions as a tumor suppressor in human non-small cell lung cancer by targeting SLC22A18

Zhang, Bicheng; Liu, Tao; Wu, Tingting; Wang, Zhigang; Rao, Zhiguo; Gao, Jian‐Fei

doi:10.1016/j.ijbiomac.2014.12.002

Cited by 55 publications

(46 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This gene has been shown to be involved in placental growth [31] and its overexpression led to low birth weight in humans [32]. The paternally expressed DIRAS3 and maternally expressed SLC22A18 are inhibitors for cell proliferation and growth [33,34], and were both downregulated in lungs of the Res group and kidneys of the Over group compared to controls, respectively. Interestingly, three of the four affected genes – PHLDA2, SLC22A18 , and IGF2 – are located near the imprinted cluster of KCNQ1 and IGF2/H19 on chromosome 21, indicating this domain is highly responsive to maternal diet changes.…”

Section: Resultsmentioning

confidence: 99%

Effects of maternal nutrition on the expression of genomic imprinted genes in ovine fetuses

et al. 2018

View full text Add to dashboard Cite

Genomic imprinting is an epigenetic phenomenon of differential allelic expression based on parental origin. To date, 263 imprinted genes have been identified among all investigated mammalian species. However, only 21 have been described in sheep, of which 11 are annotated in the current ovine genome. Here, we aim to i) use DNA/RNA high throughput sequencing to identify new monoallelically expressed and imprinted genes in day 135 ovine fetuses and ii) determine whether maternal diet (100%, 60%, or 140% of National Research Council Total Digestible Nutrients) influences expression of imprinted genes. We also reported strategies to solve technical challenges in the data analysis pipeline. We identified 80 monoallelically expressed, 13 new putative imprinted genes, and five known imprinted genes in sheep using the 263 genes stated above as a guide. Sanger sequencing confirmed allelic expression of seven genes, CASD1, COPG2, DIRAS3, INPP5F, PLAGL1, PPP1R9A, and SLC22A18. Among the 13 putative imprinted genes, five were localized in the known sheep imprinting domains of MEST on chromosome 4, DLK1/GTL2 on chromosome 18 and KCNQ1 on chromosome 21, and three were in a novel sheep imprinted cluster on chromosome 4, known in other species as PEG10/SGCE. The expression of DIRAS3, IGF2, PHLDA2, and SLC22A18 was altered by maternal diet, albeit without allelic expression reversal. Together, our results expanded the list of sheep imprinted genes to 34 and demonstrated that while the expression levels of four imprinted genes were changed by maternal diet, the allelic expression patterns were un-changed for all imprinted genes studied.

show abstract

Section: Resultsmentioning

confidence: 99%

Effects of maternal nutrition on the expression of genomic imprinted genes in ovine fetuses

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Therefore, the underlying mechanisms of cell death in NSCLC should be explored to give rise to new therapeutic strategies. Recently, the involvement of microRNAs (miRNAs) in the biology and therapy of lung cancer has been a topic of intense research [9, 10]. …”

Section: Introductionmentioning

confidence: 99%

Effect of microRNA-135a on Cell Proliferation, Migration, Invasion, Apoptosis and Tumor Angiogenesis Through the IGF-1/PI3K/Akt Signaling Pathway in Non-Small Cell Lung Cancer

Zhou

et al. 2017

Cell Physiol Biochem

113

View full text Add to dashboard Cite

Objective: This study explored the ability of microRNA-135a (miR-135a) to influence cell proliferation, migration, invasion, apoptosis and tumor angiogenesis through the IGF-1/PI3K/Akt signaling pathway in non-small cell lung cancer (NSCLC). Methods: NSCLC tissues and adjacent normal tissues were collected from 138 NSCLC patients. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression levels of miR-135a and IGF-1, PI3K, Akt, VEGF, bFGF and IL-8 mRNA; western blotting was used to determine the expression levels of IGF-1, PI3K and Akt protein; and enzyme-linked immunosorbent assay (ELISA) was used to analyze the expression levels of VEGF, bFGF and IL-8 protein. Human NSCLC cell lines (A549, H460, and H1299) and the human bronchial epithelial cell line (HBE) were selected. A549 cells were assigned to blank, negative control (NC), miR-135a mimics, miR-135a inhibitors, IGF-1 siRNA and miR-135a inhibitors + IGF-1 siRNA groups. The following were performed: an MTT assay to assess cell proliferation, a scratch test to detect cell migration, a Transwell assay to measure cell invasion, and a flow cytometry to analyze cell apoptosis. Results: The expression level of miR-135a was lower while those of IGF-1, PI3K and Akt mRNA were higher in NSCLC tissues than in the adjacent normal tissues. Dual-luciferase reporter assay indicated IGF-1 as a target of miR-135a. The in vitro results showed that compared with the blank group, cell proliferation, migration and invasion were suppressed, mRNA and protein levels of IGF-1, PI3K, Akt, VEGF, bFGF and IL-8 were reduced, and cell apoptosis was enhanced in the miR-135a mimics and IGF-1 siRNA groups. Compared with the IGF-1 siRNA group, cells in the miR-135a inhibitors + IGF-1 siRNA group demonstrated increased cell proliferation, migration and invasion, elevated mRNA and protein levels of IGF-1, PI3K, Akt, VEGF, bFGF and IL-8 and reduced cell apoptosis. Conclusion: These findings indicated that miR-135a promotes cell apoptosis and inhibits cell proliferation, migration, invasion and tumor angiogenesis by targeting IGF-1 gene through the IGF-1/PI3K/Akt signaling pathway in NSCLC.

show abstract

“…There has been a focus on identifying various tumor suppressor genes and oncogenes regulated by miRNAs in lung cancer, which can effect cancer cell survival and proliferation, such as solute carrier family 22 member 18 (SLC22A18) (15), KIT proto-oncogene receptor tyrosine kinase (16), kruppel like factor 8 (17), epidermal growth factor receptor and MET proto-oncogene receptor tyrosine kinase (18). Novel oncogenes and tumor suppressor genes are continuously being identified.…”

Section: Introductionmentioning

confidence: 99%

miR-137 inhibits the proliferation of human non-small cell lung cancer cells by targeting SRC3

Chen

Zhang

et al. 2017

Oncology Letters

View full text Add to dashboard Cite

Abstract. Non-small cell lung cancer (NSCLC) is the most common type of lung cancer. The results of the present study demonstrate that high expression of microRNA (miR)-137 and low expression of steroid receptor coactivator-3 (SRC3) had a significant negative correlation in 40 NSCLC tissue samples. In addition, cell colony formation and proliferation was significantly reduced in miR-137-transfected A549 and NCI-H838 cells compared with scramble-transfected NSCLC cell lines. miR-137 was identified to induce G 1 /S cell cycle arrest and dysregulate the mRNA expression of cell cycle-associated proteins (proliferating cell nuclear antigen, cyclin E, cyclin A1, cyclin A2 and p21) in NSCLC cells. Notably, miR-137 could significantly suppress SRC3 3' untranslated region (UTR) luciferase-reporter activity, an effect that was not detectable when the putative 3'-UTR target-site was mutated, further clarifying the molecular mechanisms underlying the role of miR-137 in NSCLC. In conclusion, the results of the present study suggest that miR-137 suppresses NSCLC cell proliferation by partially targeting SRC3.

show abstract

microRNA-137 functions as a tumor suppressor in human non-small cell lung cancer by targeting SLC22A18

Cited by 55 publications

References 26 publications

Effects of maternal nutrition on the expression of genomic imprinted genes in ovine fetuses

Effects of maternal nutrition on the expression of genomic imprinted genes in ovine fetuses

Effect of microRNA-135a on Cell Proliferation, Migration, Invasion, Apoptosis and Tumor Angiogenesis Through the IGF-1/PI3K/Akt Signaling Pathway in Non-Small Cell Lung Cancer

miR-137 inhibits the proliferation of human non-small cell lung cancer cells by targeting SRC3

Contact Info

Product

Resources

About