TGF beta1 and related-Smads contribute to pulmonary metastasis of hepatocellular carcinoma in mice model

Li, Guocai; Ye, Qing–Hai; Dong, Qiongzhu; Ren, Ning; Jia, Hongyan; Qin, Lun–Xiu

doi:10.1186/1756-9966-31-93

Cited by 17 publications

(12 citation statements)

References 31 publications

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“…The occurrence of EMT is accompanied by the altered expression of molecular markers; thus, EMT can be determined by detecting the expression of these molecular markers [ 32 ]. Different expression levels of HODX9 lead to different cell status.…”

Section: Discussionmentioning

confidence: 99%

HOXD9 promotes epithelial–mesenchymal transition and cancer metastasis by ZEB1 regulation in hepatocellular carcinoma

et al. 2015

J Exp Clin Cancer Res

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Hepatocellular carcinoma (HCC) is a common malignant tumor that severely threatens human health. The poor prognosis of HCC is mainly attributed to intrahepatic and extrahepatic metastases. HOXD9 proteins belong to a superfamily that regulates the development and control of many cellular processes, including proliferation, apoptosis, cell shape, and cell migration. HOXD9 can also function as an oncogene in several cancer cells. However, its biological function in human HCC requires further investigation. In this study, HOXD9 exhibited high expression in invasive HCC cells. HOXD9 overexpression can significantly enhance HCC cell migration, invasion, and metastasis, whereas silencing HOXD9 inhibits these processes. HOXD9 also promotes the epithelial–mesenchymal transition (EMT) of HCC cells. Microarray analysis suggests that ZEB1 can function as a downstream factor of HOXD9. HOXD9 can interact with the promoter region of ZEB1 and promotes ZEB1 expression. ZEB1 knockdown inhibits HOXD9-induced migration and invasion, as well as EMT in HCC cells. This study helps elucidates the oncogenic functions of HOXD9 in HCC.Electronic supplementary materialThe online version of this article (doi:10.1186/s13046-015-0245-3) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

HOXD9 promotes epithelial–mesenchymal transition and cancer metastasis by ZEB1 regulation in hepatocellular carcinoma

et al. 2015

J Exp Clin Cancer Res

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“…Of the metastasis-related genes, TGFB1 and EGFR had the largest number of co-occurring genes (34 and 33, respectively) and were located in the centre of the network. As recognised dysregulated growth factors, TGFB1/EGFR and their downstream signalling pathway components contribute to the proliferation and invasive behaviour of liver cancer cells [ 19 – 21 ]. As a transmembrane glycoprotein, CD44 was shown to interact with 28 genes.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics analysis of the gene expression profile of hepatocellular carcinoma: preliminary results

Li¹,

Huang²,

Wei³

2016

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Aim of the studyTo analyse the expression profile of hepatocellular carcinoma compared with normal liver by using bioinformatics methods.Material and methodsIn this study, we analysed the microarray expression data of HCC and adjacent normal liver samples from the Gene Expression Omnibus (GEO) database to screen for differentially expressed genes. Then, functional analyses were performed using GenCLiP analysis, Gene Ontology categories, and aberrant pathway identification. In addition, we used the CMap database to identify small molecules that can induce HCC.ResultsOverall, 2721 differentially expressed genes (DEGs) were identified. We found 180 metastasis-related genes and constructed co-occurrence networks. Several significant pathways, including the transforming growth factor β (TGF-β) signalling pathway, were identified as closely related to these DEGs. Some candidate small molecules (such as betahistine) were identified that might provide a basis for developing HCC treatments in the future.ConclusionsAlthough we functionally analysed the differences in the gene expression profiles of HCC and normal liver tissues, our study is essentially preliminary, and it may be premature to apply our results to clinical trials. Further research and experimental testing are required in future studies.

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“…The TGF-β signaling pathway has also been considered as a promoter of tumor progression and invasion. In response to elevated TGF-β levels, the tumor cell becomes more migratory and invasive [ 21 , 22 ]. BMP4 is up-regulated in human colonic adenocarcinoma and human colorectal cancer.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of TMEM158 contributes to ovarian carcinogenesis

Cheng

Guo

Chen

et al. 2015

J Exp Clin Cancer Res

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BackgroundTransmembrane protein 158 (TMEM158) is a recently identified upregulated gene during Ras-induced senescence. Its association with various cancers has been recently reported. However, the expression and biological function of TMEM158 in ovarian cancer is still unclear. This study was aimed to elucidate the roles of TMEM158 in cell proliferation, adhesion and cell invasion of ovarian cancer cells.MethodsWe analyzed TMEM158 mRNA level in ovarian cancer tissues and adjacent no-tumorous tissues by real-time PCR. We then suppressed TMEM158 expression of ovarian cancer cells by RNA interference and examined the effects of TMEM158 knockdown on cancerous transformation of ovarian cancer cells.ResultsThe RNA-sequencing data of the ovarian cancer cohort from The Cancer Genome Atlas project (TCGA) and our real-time PCR data showed that TMEM158 was overexpressed in ovarian cancer. Knockdown of TMEM158 by RNA interference in ovarian cancer cells significantly inhibited cell proliferation, which may be due to the increase of G1-phase arrest. Silencing of TMEM158 also inhibited cell adhesion, cell invasion as well as tumorigenicity in nude mice. Moreover, knockdown of TMEM158 notably repressed cell adhesion via down-regulating the expression intercellular adhesion molecule1 (ICAM1) and vascular cell adhesion molecule1 (VCAM1). Transforming Growth Factor-β (TGF-β) signaling pathway was also remarkably impaired by TMEM158 silencing.ConclusionsOur data suggests that TMEM158 may work as an oncogene for ovarian cancer and that inhibition of TMEM158 may be a therapeutic strategy for ovarian cancer.

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TGF beta1 and related-Smads contribute to pulmonary metastasis of hepatocellular carcinoma in mice model

Cited by 17 publications

References 31 publications

HOXD9 promotes epithelial–mesenchymal transition and cancer metastasis by ZEB1 regulation in hepatocellular carcinoma

HOXD9 promotes epithelial–mesenchymal transition and cancer metastasis by ZEB1 regulation in hepatocellular carcinoma

Bioinformatics analysis of the gene expression profile of hepatocellular carcinoma: preliminary results

Overexpression of TMEM158 contributes to ovarian carcinogenesis

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