miR-182 suppresses invadopodia formation and metastasis in non-small cell lung cancer by targeting cortactin gene

Li, Yongwen; Zhang, Hongbing; Gong, Hao; Yin, Yuan; Liu, Ying; Wang, Cong; Li, Weiting; Zhang, Zihe; Liu, Minghui; Liu, Hongyu; Chen, Jun

doi:10.1186/s13046-018-0824-1

Cited by 52 publications

(42 citation statements)

References 44 publications

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“…CTTN has been confirmed as an oncogene and positive regulator of metastasis by previous study [ 25 – 27 ]. By bioinformatics predict that CTTN was a target gene of piR-19166 and there is one complementary binding site between piR-19166 and CTTN 3’UTR region.…”

Section: Discussionmentioning

confidence: 85%

piR-19166 inhibits migration and metastasis through CTTN/MMPs pathway in prostate carcinoma

Cao

Sun

et al. 2020

Aging

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Tumor metastasis is one of death causes for patients of prostate carcinoma. PIWI-interacting RNAs (piRNAs) are a subtype of noncoding protein RNAs that are involved in tumorigenesis, but the effect of piRNAs in prostate carcinoma (PCa) remains unclear. This article showed the identification of piRNAs was performed using a piRNA microarray screen in PCa tissues and several piRNAs were identified as dysregulated. The two up-regulated piRNAs (piR-19004 and piR-2878) and one down-regulated piR-19166 have been validated in the tissues and cell lines of PCa using quantitative reverse transcription polymerase chain reaction (qRT-PCR). Further studies showed that piR-19166 is transfected into PCa cells to suppress its migration and metastasis. Mechanistically, cortactin (CTTN) 3' untranslated region (UTR) was complementary combined with piR-19166 by bioinformatic prediction and identified as a direct target of piR-19166 through dual-luciferase reporter assay. Over-expression and knockdown of CTTN could respectively rescue and simulate the effects induced by piR-19166. Finally, piR-19166 suppresses migration and metastasis by the CTTN/matrix metalloproteinases (MMPs) pathway in PCa cells. Thus, these findings suggested that piR-19166 targets the CTTN of prostate cancer cells to inhibit migration and distant metastasis, and may represent a new marker of diagnosis and treatment for PCa patients in early stages.

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Section: Discussionmentioning

confidence: 85%

piR-19166 inhibits migration and metastasis through CTTN/MMPs pathway in prostate carcinoma

Cao

Sun

et al. 2020

Aging

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“…Recently, numerous researches have shown that the degradation of extracellular matrix and basement membrane plays a decisive role in the invasion and metastasis of cancer cells. [ 15 – 17 ] Cell adhesion is the key to invasion and metastasis of cancer. [ 18 , 19 ] Increasing number of researches and experiments have found that cell adhesion molecules are closely linked to lung cancer.…”

Section: Discussionmentioning

confidence: 99%

Identification of crucial genes associated with lung adenocarcinoma by bioinformatic analysis

Dai¹,

Zhou²,

Wang³

2020

Medicine

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Lung cancer is the world's most common malignancies and ranks first among all cancer-related deaths. Lung adenocarcinoma (LUAD) is the most frequent histological type in lung cancer. Its pathogenesis has not yet been fully elucidated, so it is of great significance to explore related genes for elucidating the molecular mechanism involved in occurrence and development of LUAD. To explore the crucial genes associated with LUAD development and progression, microarray datasets GSE7670, GSE10072, and GSE31547 were acquired from the Gene Expression Omnibus (GEO) database. R language Limma package was adopted to screen the differentially expressed genes (DEGs). The clusterProfiler package was used for enrichment analysis and annotation of the Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genome (KEGG) pathways for DEGs. The Search Tool for the Retrieval of Interacting Genes database (STRING) was used to construct the protein interaction network for DEGs, while Cytoscape was adopted to visualize it. The functional module was screened with Cytoscape's MCODE (The Molecular Complex Detection) plugin. The crucial genes associated with LUAD were identified by cytoHubba plugin. Kaplan–Meier plotter online tool was used to perform survival analysis of the hub gene. Three hundred twenty-one DEGs in total were screened, of which 105 were upregulated and 216 were downregulated. It was found that some GO terms and pathways (e.g., collagen trimer, extracellular structure organization, heparin binding, complement and coagulation cascades, malaria, protein digestion and absorption, and PPAR signaling pathway) were considerably enriched in DEGs. UBE2C, TOP2A, RRM2, CDC20, CCNB2, KIAA0101, BUB1B, TPX2, PRC1, and CDK1 were identified as crucial genes. Survival analysis showed that the overexpression of UBE2C, TOP2A, RRM2, CDC20, CCNB2, KIAA0101, BUB1B, TPX2, and PRC1 significantly reduced the overall survival of LUAD patients. One of the crucial genes: UBE2C was validated by immunohistochemistry to be upregulated in LUAD tissues. This study screened out potential biomarkers of LUAD, providing a theoretical basis for elucidating the pathogenesis and evaluating the prognosis of LUAD.

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“…Previous studies have shown that Src protein and RNA expression levels are significantly upregulated in most HBV + -HCC specimens and HBx transgenic mice, and the overexpression of Src promotes cell viability, migration, and cell colony formation [34][35][36] . The Src substrate CTTN has been found to be overexpressed in various cancers, including human colorectal cancer, esophageal tumors, and non-small-cell lung cancer, and HCC and CTTN overexpression closely correlates with tumor aggressiveness, cell adhesion, and cell motility [37][38][39][40][41][42] . We demonstrated that HBx contributed to cell migration and proliferation of HCC by binding CTTN in the cytoplasm and upregulating its expression.…”

Section: Discussionmentioning

confidence: 99%

The HBx–CTTN interaction promotes cell proliferation and migration of hepatocellular carcinoma via CREB1

et al. 2019

Cell Death Dis

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Hepatitis B virus-encoded X protein (HBx) acts as a tumor promoter during hepatocellular carcinoma (HCC) development, probably by regulating the expression of host proteins through protein-protein interaction. A proteomics approach was used to identify HBx-interacting proteins involved in HBx-induced hepatocarcinogenesis. We validated the proteomics findings by co-immunoprecipitation and confocal microscopy. We performed cell proliferation, migration assays and cell cycle analyses in HCC cells. Finally, we confirmed the clinical significance of our findings in samples from patients. We found that cortactin (CTTN) is a novel HBx-interacting protein, and HBx regulates the expression of CTTN in the HCC cell lines MHCC-LM3 and HepG2. Mechanistically, by upregulating the expression of cAMP response element-binding protein (CREB1) and its downstream targets, such as cyclin D1 and MMP-9, the effects of the HBx-CTTN interaction on the enhancement of cellular proliferation and migration were maintained by inhibiting cell cycle arrest. In addition, we demonstrated that the levels of CTTN and CREB1 were closely correlated in clinical samples from HBV-infected patients with HCC. Overall, our data suggests that HBx contributes to cell migration and proliferation of HCC cells by interacting with CTTN and regulating the expression of CTTN and CREB1. Therefore, the HBx/CTTN/CREB1 axis is a potential novel therapeutic target in HCC.

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miR-182 suppresses invadopodia formation and metastasis in non-small cell lung cancer by targeting cortactin gene

Cited by 52 publications

References 44 publications

piR-19166 inhibits migration and metastasis through CTTN/MMPs pathway in prostate carcinoma

piR-19166 inhibits migration and metastasis through CTTN/MMPs pathway in prostate carcinoma

Identification of crucial genes associated with lung adenocarcinoma by bioinformatic analysis

The HBx–CTTN interaction promotes cell proliferation and migration of hepatocellular carcinoma via CREB1

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