MicroRNA in lung cancer

Py, Lin; Yu, Sung-Liang; Yang, Pan‐Chyr

doi:10.1038/sj.bjc.6605901

Cited by 207 publications

(148 citation statements)

References 64 publications

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“…20 MiRNA expression profiles of NSCLC have also been reported by many researchers. 21,22 However, few studies describe similar analysis of lung-SCC, one of the most lethal malignancies in the world, with a 5-year survival rate of approximately 60% after curative surgery. Increased understanding of the molecular pathways involved in lung-SCC carcinogenesis would help improve diagnosis and therapy of the disease.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have revealed that the normal regulatory mechanisms in these cancer pathways are disrupted by aberrant expression of microRNA (miRNA). 8 MiRNAs are a class of small non-coding RNA molecules consisting of [19][20][21][22] nucleotides that regulate gene expression through translational repression and mRNA cleavage, 8 and have an important role in a variety of biological processes, including development, differentiation, apoptosis and cell proliferation. Bioinformatic predictions indicate that miRNAs regulate more than 30% of protein coding genes.…”

Section: Introductionmentioning

confidence: 99%

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Tumor suppressive microRNA-133a regulates novel molecular networks in lung squamous cell carcinoma

et al. 2011

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Analysis of the microRNA (miRNA) expression signature of lung squamous cell carcinoma (lung-SCC) revealed that the expression levels of miR-133a were significantly reduced in cancer tissues compared with normal tissues. In this study, we focused on the functional significance of miR-133a in cancer cell lines derived from lung-SCC and the identification of miR133a-regulated novel cancer networks in lung-SCC. Restoration of miR-133a expression in PC10 and H157 cell lines resulted in significant inhibition of cell proliferation, suggesting that miR-133a functions as a tumor suppressor. We used genome-wide gene expression analysis to identify the molecular targets of miR-133a regulation. Gene expression data and web-based searching revealed several candidate genes, including transgelin 2 (TAGLN2), actin-related protein2/3 complex, subunit 5, 16kDa (ARPC5), LAG1 homolog, ceramide synthase 2 (LASS2) and glutathione S-transferase pi 1 (GSTP1). ARPC5 and GSTP1 likely represent bona fide targets as their expression is elevated in lung-SCC clinical specimens. Furthermore, transient transfection of miR-133a, repressed ARPC5 and GSTP1 mRNA and protein levels. As cell proliferation was significantly inhibited in lung-SCC cells following RNAi knock down of either gene, ARPC5 and GSTP1 may function as oncogenes in the development of lung-SCC. The identification of a tumor suppressive miRNA and the novel cancer pathways it regulates could provide new insights into potential molecular mechanisms of lung-SCC carcinogenesis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Tumor suppressive microRNA-133a regulates novel molecular networks in lung squamous cell carcinoma

et al. 2011

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“…Many miRNAs have been reported to be associated with lung cancer cell survival and proliferation (12). However, there have been few studies focusing on the role of miRNAs in the chemoradioresistance and EMT of lung cancer.…”

Section: Introductionmentioning

confidence: 99%

Let-7c Governs the Acquisition of Chemo- or Radioresistance and Epithelial-to-Mesenchymal Transition Phenotypes in Docetaxel-Resistant Lung Adenocarcinoma

Cui

Huang

Chen

et al. 2013

Molecular Cancer Research

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MicroRNA (miRNA) expression and functions have been reported to contribute to phenotypic features of tumor cells. Although targets and functional roles for many miRNAs have been described in lung adenocarcinoma (LAD), their pathophysiologic roles in phenotypes of chemoresistant LAD cells are still largely unclear. Previously, docetaxel (DTX)-resistant LAD cell lines (SPC-A1/DTX and H1299/DTX) were established by our laboratory and displayed chemo-or radioresistance and mesenchymal features with enhanced invasiveness and motility. Unbiased miRNA profiling indicated that let-7c (MIRLET7C) was significantly downregulated in SPC-A1/DTX cells. Ectopic let-7c expression increased the in vitro and in vivo chemo-or radiosensitivity of DTX-resistant LAD cells through enhanced apoptosis, reversal of epithelial-tomesenchymal phenotypes, and inhibition of in vivo metastatic potential via inactivation of Akt phosphorylation, whereas a let-7c inhibitor decreased the chemo

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“…For example, miR-126 impacts endothelial recruitment by modulating the IGF1/IGF1R and GAS6/MERK pathways 5 . Recent studies have also shown that dysregulation of miRNAs is involved in carcinogenesis and metastasis in several human cancer types [6][7][8] .…”

mentioning

confidence: 99%

“…Several miRNAs, including miR-126, miR-21 and miR-335, have been associated with metastasis in several types of cancers 7,10,11 . To study the role of miRNA in lung cancer metastasis, we first established a series of lung adenocarcinoma cell sub-lines with increasing invasive and metastatic abilities 12 .…”

mentioning

confidence: 99%

MicroRNA-135b promotes lung cancer metastasis by regulating multiple targets in the Hippo pathway and LZTS1

et al. 2013

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Dysregulation of microRNAs has a critical role in cancer progression. Here we identify an intronic microRNA, miR-135b that is upregulated in highly invasive non-small-cell lung cancer cells. Expression of miR-135b enhances cancer cell invasive and migratory abilities in vitro and promotes cancer metastasis in vivo, while specific inhibition of miR-135b by a miR-135b-specific molecular sponge and antagomirs suppresses cancer cell invasion, orthotopic lung tumour growth and metastasis in a mouse model. miR-135b targets multiple key components in the Hippo pathway, including LATS2, b-TrCP and NDR2, as well as LZTS1. Expression of miR-135b, LZTS1, LATS2 and nuclear TAZ predicts poor outcomes of non-small-cell lung cancer. We find that miR-135b is dually regulated by DNA demethylation and nuclear factor-kappaB signalling, implying that abnormal expression of miR-135b in cancer may result from inflammatory and epigenetic modulations. We conclude that miR-135b is an oncogenic microRNA and a potential therapeutic target for non-small-cell lung cancer.

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MicroRNA in lung cancer

Cited by 207 publications

References 64 publications

Tumor suppressive microRNA-133a regulates novel molecular networks in lung squamous cell carcinoma

Tumor suppressive microRNA-133a regulates novel molecular networks in lung squamous cell carcinoma

Let-7c Governs the Acquisition of Chemo- or Radioresistance and Epithelial-to-Mesenchymal Transition Phenotypes in Docetaxel-Resistant Lung Adenocarcinoma

MicroRNA-135b promotes lung cancer metastasis by regulating multiple targets in the Hippo pathway and LZTS1

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