EMMPRIN silencing inhibits proliferation and perineural invasion of human salivary adenoid cystic carcinoma cells in vitro and in vivo

Yang, Xinjie; Zhang, Pu; Ma, Qin; Kong, Liang; Li, Yuan; Liu, Baolin; Lei, Delin

doi:10.4161/cbt.13.2.18455

Cited by 27 publications

(18 citation statements)

References 33 publications

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“…Proteins involved in cell-cell adhesion (hemidesmosome proteins B180 and B230, E-and N-cadherin, CDH12, acatenin, mammalian ENA, CD44 and CD24) [93][94][95][96][97][98], migration (matrix metalloproteinase, heparanase, CD147 or extracellular matrix metalloproteinase inducer or Emmprin) [11,[99][100][101][102] and epithelial-mesenchymal transition (NBS-1 and snail)…”

Section: Proteins Involved In Apoptosismentioning

confidence: 99%

Molecular Markers and Chemotherapy for Advanced Salivary Cancer

Poorten

Meulemans

Delaere

et al. 2014

Curr Otorhinolaryngol Rep

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Recent advances in our understanding of the molecular biology of salivary gland neoplasms have yielded diagnostic targets and potential therapeutic targets that have started to change our approach and choice of treatment strategies. Currently, these options are mainly investigated in recurrent and metastatic salivary gland cancer (SGC). Although the results of both cytotoxic and targeted molecular biological systemic therapy for locoregional recurrence and distant spread of SGC remain largely unpredictable, targeted therapy can be the treatment of choice in selected cases today. Molecular analysis is required as part of the diagnostic workup to help select patients with recurrent and metastatic SGC who may benefit from targeted or standard treatment regimens.

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Section: Proteins Involved In Apoptosismentioning

confidence: 99%

Molecular Markers and Chemotherapy for Advanced Salivary Cancer

Poorten

Meulemans

Delaere

et al. 2014

Curr Otorhinolaryngol Rep

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“…A modified protocol of Transwell cultures was used, based on previous studies (15,16). A Transwell ® (24 mm) with a 0.4-µm pore polyester membrane insert (Corning, Inc., Corning, NY, uSA) was used to establish the co-culture system.…”

Section: Establishment Of a Co-culture System Between Tumor Cells Andmentioning

confidence: 99%

Schwann cells promote EMT and the Schwann-like differentiation of salivary adenoid cystic carcinoma cells via the BDNF/TrkB axis

et al. 2015

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Abstract. Perineural invasion (PNI) is a striking biological behavior observed in salivary adenoid cystic carcinoma (SACC). The present study was designed to establish a co-culture model of SACC cells with Schwann cells (SCs), and then study epithelial-mesenchymal transition (EMT) and the Schwann-like differentiation of SACC cells to investigate the likely molecular mechanism of PNI. The co-culture models of SCs with tumor cells (SACC-83, SACC-LM and MEC-1) were established using a Transwell system. An elevated concentration of brain-derived neurotrophic factor (BDNF) was detected by ELISA assay in the co-cultured medium of the SACC-83 group and SACC-LM group rather than the MEC-1 group. The EMT process and Schwann-like differentiation in SACC-83 cells were analyzed by RT-PCR, western blotting, immunofluorescence, photography, and migration and perineural invasion assays. The SACC-83 cells under the co-culture condition with SCs changed to a mesenchymal morphology and had higher migration and invasion capabilities compared with the solely cultured SACC-83 cells, accompanied by the downregulation of E-cadherin and upregulation of N-cadherin and vimentin. The co-cultured SACC-83 cells also developed Schwann-like differentiation with increased expression of SC markers, S100A4 and GFAP. However, inhibition of tropomyosin-related kinase B (TrkB) by K252a markedly blocked these effects. Additionally, the expression and correlation of TrkB, E-cadherin and S100A4 were analyzed by immunohistochemistry in 187 primary SACC cases. The levels of TrkB and S100A4 expression were both positively associated with PNI in the SACC cases, while E-cadherin expression was negatively associated with PNI. Elevated expression of TrkB was significantly correlated with the downregulated expression of E-cadherin and the upregulated expression of S100A4 in the SACC cases. Our results suggest that SCs play a pivotal role in the PNI process by inducing the EMT process and the Schwann-like differentiation of SACC cells via the BDNF/TrkB axis. Interruption of the interreaction between SACC cells and SCs by targeting the BDNF/TrkB axis may be a potential strategy for anti-PNI therapy in SACC.

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“…On the other hand, it was demonstrated that silencing of gal-3 in gastric cancer cells downregulated the expression level of MMP-1 and 9 [Kim et al, 2011]. It was shown that silencing of EMMPRIN expression in the human SACC cell line (Salivary adenoid cystic carcinoma) suppressed MMP-2 and MMP-9 secretion [Yang et al, 2012]. Silencing gal-3 in pancreatic cancer cells reduced MMP-2 expression via the Wnt signaling pathway [Kobayashi et al, 2011].…”

Section: Discussionmentioning

confidence: 99%

Runt‐Related Transcription Factor 2 (Runx2) Is Responsible for Galectin‐3 Overexpression in Human Thyroid Carcinoma

Kaptan

Baş

Sancakli

et al. 2017

J of Cellular Biochemistry

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Runx2 promotes metastatic ability of cancer cells by directly activating some of the mediators regarding malignancy. Galectin-3 (Gal-3) extensively expressed in normal and transformed cells and it is responsible for many cellular processes. In this study, we aimed to investigate whether there is any relationship between runx2 transcription factor and regulation of galectin-3 expression in different human thyroid carcinoma cell lines. To show effects of runx2 transcription factor on gal-3 expression, we developed runx2 knockdown model in the thyroid carcinoma cell lines; anaplastic 8505C and 8305C and, papillary TPC-1 and follicular FTC-133 by using siRNA transfection. We analyzed the protein expressions and mRNA levels of gal-3 and MMP2/9 in the runx2-silenced cell lines using Western blotting, qPCR, and fluorescent microscopy. Our results showed that mRNA expression levels of gal-3 and MMP2/9 were downregulated in runx2-silenced cell lines. In this investigation, we revealed that regulation of gal-3 expression was strongly correlated with runx2 transcription factor in human thyroid carcinoma. Considering the contribution of human gal-3 in collaboration with MMP2/9 to the malignant characters of many cancers, regulation of their expressions through runx2 seems like one of the key regulatory mechanism for malignant potential of human thyroid carcinoma. Accordingly, runx2 transcription factor inhibitors can be a potential target in order to prevent gal-3 mediated malignancy of human thyroid carcinoma. J. Cell. Biochem. 118: 3911-3919, 2017. © 2017 Wiley Periodicals, Inc.

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EMMPRIN silencing inhibits proliferation and perineural invasion of human salivary adenoid cystic carcinoma cells in vitro and in vivo

Cited by 27 publications

References 33 publications

Molecular Markers and Chemotherapy for Advanced Salivary Cancer

Molecular Markers and Chemotherapy for Advanced Salivary Cancer

Schwann cells promote EMT and the Schwann-like differentiation of salivary adenoid cystic carcinoma cells via the BDNF/TrkB axis

Runt‐Related Transcription Factor 2 (Runx2) Is Responsible for Galectin‐3 Overexpression in Human Thyroid Carcinoma

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