Expression profiling of supraglottic carcinoma: PTEN and thrombospondin 2 are associated with inhibition of lymphatic metastasis

Bai, Weiliang; Wang, Liping; Ji, Wenyue; Gao, Hong

doi:10.1080/00016480802294351

Cited by 12 publications

(8 citation statements)

References 19 publications

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“…For miR-335-5p, it was reported that it can suppress invasion of lung cancer cell, neuroblastoma cell and osteosarcoma cells [39][40][41] . In addtion, THBS2 is reported associated with inhibition of supraglottic carcinoma and pancreatic cancer cell invasion 42,43 . These findings partly show the correctness of the our analysis results.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive gene and microRNA expression profiling reveals miR-206 inhibits MET in lung cancer metastasis

Chen

Jiao

et al. 2015

Mol. BioSyst.

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MiRNAs associated with the metastasis of lung cancer remain largely unexplored. In this study, gene and miRNA expression profiling were performed to analyze the global expression of mRNAs and miRNAs in human high- and low-metastatic lung cancer cell strains. By developing an integrated bioinformatics analysis, six miRNAs (miR-424-3p, miR-450b-5p, miR-335-5p, miR-34a-5p, miR-302b-3p and miR-206) showed higher target gene degrees in the miRNA-gene network and might be potential metastasis-related miRNAs. Using the qRT-PCR method, the six miRNAs were further confirmed to show a significant expression difference between human lung cancer and normal tissue samples. Since miR-206 showed lower expression both in lung cancer tissues and cell lines, it was used as an example for further functional verification. The wound healing assay and transwell invasion assay showed that miR-206 mimics significantly inhibited the cell migration and invasion of the high-metastatic lung cancer 95D cell strain. One of its predicted targets in our miRNA-gene network, MET, was also obviously decreased at the protein level when miR-206 was overexpressed. Instead, miR-206 inhibitors increased MET protein expression, cell migration and invasion of the low-metastatic lung cancer 95C cell strain. Meanwhile, the luciferase assay showed that MET was a direct target of miR-206. Furthermore, MET gene silence showed a similar anti-migration and anti-invasion effect with miR-206 mimics in 95D cells and could partially attenuate the migration- and invasion-promoting effect of miR-206 inhibitors in 95C cells, suggesting that miR-206 targets MET in lung cancer metastasis. Finally, we also demonstrated that miR-206 can significantly inhibit lung cancer proliferation and metastasis in mouse models. In conclusion, our study provided a miRNA-gene regulatory network in lung cancer metastasis and further demonstrated the roles of miR-206 and MET in this process, which enhances the understanding of the regulatory mechanism in lung cancer metastasis.

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Section: Discussionmentioning

confidence: 99%

Comprehensive gene and microRNA expression profiling reveals miR-206 inhibits MET in lung cancer metastasis

Chen

Jiao

et al. 2015

Mol. BioSyst.

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“…The Ets1 transcription factor is normally expressed within the proliferative basal layer of the epidermis (Nagarajan et al, 2009), but in many squamous cell cancers, Ets1 is overexpressed in malignant keratinocytes, where its expression is correlated with invasion and metastasis (Bai et al, 2009;Endo et al, 2006;Keehn et al, 2004;Pande et al, 1999;Saeki et al, 2000;Vairaktaris et al, 2007). In order to address the potential role of Ets1 in keratinocyte biology and in the induction of squamous cell tumors, we generated a mouse model in which we can inducibly express Ets1 in keratinocytes that have already begun their differentiation process.…”

Section: Discussionmentioning

confidence: 99%

“…In normal tissues, Ets1 is expressed only in the basal layer of stratified squamous epithelium (Nagarajan et al, 2009). However, in a large fraction of SCC tumors, Ets1 is highly expressed within the malignant keratinocytes, and its levels directly correlate with the invasive and metastatic potential of the tumor (Bai et al, 2009;Endo et al, 2006;Keehn et al, 2004;Pande et al, 1999;Saeki et al, 2000;Vairaktaris et al, 2007). Tumors that express high levels of Ets1 typically also express high levels of several matrix metalloprotease (Mmp) genes (Dittmer, 2003;Hahne et al, 2008;Lincoln and Bove, 2005) and Ets1 has been shown to directly regulate expression of multiple Mmp genes (Baillat et al, 2006;Nagarajan et al, 2009;Ozaki et al, 2000;Reisdorff et al, 2002;Wei et al, 2009;Westermarck et al, 1997).…”

Section: Ets1 Blocks Terminal Differentiation Of Keratinocytes and Inmentioning

confidence: 99%

Ets1 blocks terminal differentiation of keratinocytes and induces expression of matrix metalloproteases and innate immune mediators

Nagarajan

Chin

Wang

et al. 2010

Journal of Cell Science

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SummaryThe transcription factor Ets1 is normally expressed in the proliferative layer of stratified epithelium, but expression of Ets1 is significantly upregulated in squamous cell carcinomas. How elevated levels of Ets1 impact tumor initiation and progression is not well understood. To determine the biological consequences of overexpression of Ets1, we developed a transgenic mouse model that allows induction of Ets1 expression in keratinocytes of stratified epithelium in a regulatable fashion. Induction of Ets1 during embryonic development results in a dramatic alteration in epidermal structure and function by suppressing the expression of multiple stratum corneum constituents, while at the same time inducing expression of EGF ligands, AP1 transcription factors and matrix metalloproteases. Interestingly, expression of certain immune-related genes, including defensins, chemokines and cytokines was increased as well, suggesting a possible role for immune dysregulation in the promotion of squamous dysplasia. Experiments using cultured mouse keratinocytes indicate that Ets1 can induce expression of some of these mediators in a cell-intrinsic fashion. Collectively, our data reveal that elevated expression of Ets1 has a much broader array of pro-tumorigenic effects on epithelial cells than previously appreciated.

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“…THBS2 suppresses angiogenesis by inhibiting endothelial cell migration, inducing endothelial cell apoptosis and preventing the interaction of growth factors with the cell surface receptors of the endothelial cell . In supraglottic cancer, THBS2 gene expression seems inversely correlated with nodal metastases …”

Section: Introductionmentioning

confidence: 99%

“…9 In supraglottic cancer, THBS2 gene expression seems inversely correlated with nodal metastases. 10 TACSDT2, also known as TROP-2, belongs to a unique family of transmembrane glycoproteins that has a regulatory role in cell-cell adhesion and has a key controlling role in human cancer growth. Tumor development is quantitatively driven by TACSTD2 expression levels in many tumors.…”

Section: Introductionmentioning

confidence: 99%

Nodal metastasis and survival in oral cancer: Association with protein expression of SLPI, not with LCN2, TACSTD2, or THBS2

et al. 2014

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Expression profiling of supraglottic carcinoma: PTEN and thrombospondin 2 are associated with inhibition of lymphatic metastasis

Cited by 12 publications

References 19 publications

Comprehensive gene and microRNA expression profiling reveals miR-206 inhibits MET in lung cancer metastasis

Comprehensive gene and microRNA expression profiling reveals miR-206 inhibits MET in lung cancer metastasis

Ets1 blocks terminal differentiation of keratinocytes and induces expression of matrix metalloproteases and innate immune mediators

Nodal metastasis and survival in oral cancer: Association with protein expression of SLPI, not with LCN2, TACSTD2, or THBS2

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