The developmentally-regulated Smoc2 gene is repressed by aryl-hydrocarbon receptor (Ahr) signaling

Liu, Peijun; Pazin, Dorothy E.; Merson, Rebeka R.; Albrecht, Kenneth H.; Vaziri, Cyrus

doi:10.1016/j.gene.2008.12.010

Cited by 16 publications

(14 citation statements)

References 52 publications

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“…Previous study confirmed that Smoc2 could promote cell cycle progression of human umbilical vein endothelial cells by inducing the expression of transcripts required for cell cycle[10]. Other studies have shown that Smoc2 is necessary for DNA synthesis in the cell cycle and is likely to impact cell growth in vitro and in vivo [11].…”

Section: Introductionmentioning

confidence: 80%

Smoc2 potentiates proliferation of hepatocellular carcinoma cells via promotion of cell cycle progression

Su¹,

Kuai²,

Li³

2016

WJG

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AIMTo determine the influence of Smoc2 on hepatocellular carcinoma (HCC) cell proliferation and to find a possible new therapeutic target for preventing HCC progression.METHODSWe detected expression of Smoc2 in HCC tissues and corresponding non-tumor liver (CNL) tissues using PCR, western blot, and immunohistochemistry methods. Subsequently, we down-regulated and up-regulated Smoc2 expression using siRNA and lentivirus transfection assay, respectively. Then, we identified the effect of Smoc2 on cell proliferation and cell cycle using CCK-8 and flow cytometry, respectively. The common cell growth signaling influenced by Smoc2 was detected by western blot assay.RESULTSThe expression of Smoc2 was significantly higher in HCC tissues compared with CNL tissues. Overexpression of Smoc2 promoted HCC cell proliferation and cell cycle progression. Down-regulation of Smoc2 led to inhibition of cell proliferation and cell cycle progression. Smoc2 had positive effect on ERK and AKT signaling.CONCLUSIONSmoc2 promotes the proliferation of HCC cells through accelerating cell cycle progression and might act as an anti-cancer therapeutic target in the future.

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Section: Introductionmentioning

confidence: 80%

Smoc2 potentiates proliferation of hepatocellular carcinoma cells via promotion of cell cycle progression

Su¹,

Kuai²,

Li³

2016

WJG

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“…SMOC-2 is a matricellular protein [13][14][15]18 reported to be involved in various developmental processes, 15,18,19 in regulating the cell cycle and cyclin D1 expression in 3T3 cells, 15 angiogenic growth factor activity, 20 cell-adhesion and migration of keratinocytes (possibly via integrins), 21 and Ran GTPase-modulated 3T3 cell transformation and SKBR3 breast cancer cell invasion. 22 Recently, SMOC-2 was identified as a marker of intestinal stem cells in mice, based on its increased expression and exclusive localization in epithelial cells at the bottom of intestinal crypts in Lgr5 + stem cells.…”

Section: Discussionmentioning

confidence: 99%

Induction of the intestinal stem cell signature gene SMOC-2 is required for L1-mediated colon cancer progression

et al. 2015

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Overactivation of Wnt-β-catenin signaling, including β-catenin-TCF target gene expression, is a hallmark of colorectal cancer (CRC) development. We identified the immunoglobulin family of cell-adhesion receptors member L1 as a β-catenin-TCF target gene preferentially expressed at the invasive edge of human CRC tissue. L1 can confer enhanced motility and liver metastasis when expressed in CRC cells. This ability of L1-mediated metastasis is exerted by a mechanism involving ezrin and the activation of NF-κB target genes. In this study, we identified the secreted modular calcium-binding matricellular protein-2 (SMOC-2) as a gene activated by L1-ezrin-NF-κB signaling. SMOC-2 is also known as an intestinal stem cell signature gene in mice expressing Lgr5 in cells at the bottom of intestinal crypts. The induction of SMOC-2 expression in L1-expressing CRC cells was necessary for the increase in cell motility, proliferation under stress and liver metastasis conferred by L1. SMOC-2 expression induced a more mesenchymal like phenotype in CRC cells, a decrease in E-cadherin and an increase in Snail by signaling that involves integrin-linked kinase (ILK). SMOC-2 was localized at the bottom of normal human colonic crypts and at increased levels in CRC tissue with preferential expression in invasive areas of the tumor. We found an increase in Lgr5 levels in CRC cells overexpressing L1, p65 or SMOC-2, suggesting that L1-mediated CRC progression involves the acquisition of a stem cell-like phenotype, and that SMOC-2 elevation is necessary for L1-mediated induction of more aggressive/invasive CRC properties.

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“…In the embryonic murine lung, Smoc2 signals are present in the developing smooth muscle of pulmonary artery and airways (PL, JL, WVC, and CV, unpublished observations). Smoc2 is a transcriptional target of activated aryl-hydrocarbon receptor, which mediates the adverse effects of environmental arylhydrocarbon exposure (22,23). SMOC2 expression in COPD has not been reported.…”

Section: Smoc2 Airway Development and Copdmentioning

confidence: 99%

Mechanisms of Lung Development: Contribution to Adult Lung Disease and Relevance to Chronic Obstructive Pulmonary Disease

Shi¹,

Chen²,

Cardoso³

2009

Proceedings of the American Thoracic Society

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The developmentally-regulated Smoc2 gene is repressed by aryl-hydrocarbon receptor (Ahr) signaling

Cited by 16 publications

References 52 publications

Smoc2 potentiates proliferation of hepatocellular carcinoma cells via promotion of cell cycle progression

Smoc2 potentiates proliferation of hepatocellular carcinoma cells via promotion of cell cycle progression

Induction of the intestinal stem cell signature gene SMOC-2 is required for L1-mediated colon cancer progression

Mechanisms of Lung Development: Contribution to Adult Lung Disease and Relevance to Chronic Obstructive Pulmonary Disease

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