Pleiotrophin and N-syndecan promote perineural invasion and tumor progression in an orthotopic mouse model of pancreatic cancer

Yao, Jun; Zhang, Lulin; Huang, Xu-Mei; Li, Wenyao; Gao, Shegan

doi:10.3748/wjg.v23.i21.3907

Cited by 22 publications

(14 citation statements)

References 34 publications

(32 reference statements)

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“…Whether SDC3-mediated regulation of MSC migration is directly linked to SDC3-mediated regulation of adhesion or via other pathways, remains to be established. In other cell types SDC3 regulates migration by functioning as a ligand for the soluble factor heparinbinding growth-associated molecule (HB-GAM) also known as pleiotrophin 43,44 . However, pleiotrophin failed to enhance migration of both wild type and Sdc3 −/− MSCs in our transwell assays, suggesting that, at least under our experimental conditions, SDC3-mediated regulation of MSC migration is not pleiotrophin-dependent.…”

Section: Discussionmentioning

confidence: 99%

Syndecan-3 regulates MSC adhesion, ERK and AKT signalling in vitro and its deletion enhances MSC efficacy in a model of inflammatory arthritis in vivo

Jones¹,

Stefan²,

Kay³

et al. 2020

Sci Rep

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Rheumatoid arthritis (RA) is a debilitating and painful inflammatory autoimmune disease characterised by the accumulation of leukocytes in the synovium, cartilage destruction and bone erosion. The immunomodulatory effects of bone marrow derived mesenchymal stem cells (MSCs) has been widely studied and the recent observations that syndecan-3 (SDC3) is selectively pro-inflammatory in the joint led us to hypothesise that SDC3 might play an important role in MSC biology. MSCs isolated from bone marrow of wild type and Sdc3−/− mice were used to assess immunophenotype, differentiation, adhesion and migration properties and cell signalling pathways. While both cell types show similar differentiation potential and forward scatter values, the cell complexity in wild type MSCs was significantly higher than in Sdc3−/− cells and was accompanied by lower spread surface area. Moreover, Sdc3−/− MSCs adhered more rapidly to collagen type I and showed a dramatic increase in AKT phosphorylation, accompanied by a decrease in ERK1/2 phosphorylation compared with control cells. In a mouse model of antigen-induced inflammatory arthritis, intraarticular injection of Sdc3−/− MSCs yielded enhanced efficacy compared to injection of wild type MSCs. In conclusion, our data suggest that syndecan-3 regulates MSC adhesion and efficacy in inflammatory arthritis, likely via induction of the AKT pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Syndecan-3 regulates MSC adhesion, ERK and AKT signalling in vitro and its deletion enhances MSC efficacy in a model of inflammatory arthritis in vivo

Jones¹,

Stefan²,

Kay³

et al. 2020

Sci Rep

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show abstract

“…Pleiotrophin (PTN) is a small heparin-binding cytokine which can be induced during tumorigenesis (31). Levels of PTN have been found to be increased in several cancer cell lines and primary tumors, including pancreatic cancer (32), hepatocellular carcinoma (33), breast (34) and papillary thyroid cancer (35). PTN promotes tumor progression either through direct effects on tumor cells or through stimulation of angiogenesis and remodeling of the tumor microenvironment (36–38).…”

Section: Discussionmentioning

confidence: 99%

Luteolin suppresses colorectal cancer cell metastasis via regulation of the miR‑384/pleiotrophin axis

et al. 2019

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Luteolin (3,4,5,7-tetrahydroxyflavone) is a natural flavonoid that has been found to exhibit anticancer properties in certain types of cancers. In the present study, the role of luteolin and its underlying mechanisms were explored in colorectal cancer (CRC) cells. First, the effects of luteolin on CRC cells proliferation, migration and invasion were examined by CCK-8, wound healing and Transwell assays, respectively. It was demonstrated that luteolin had no effects on CRC cells proliferation while inhibited cells migration and invasion both in vitro and in vivo . Then, expression of pleiotrophin (PTN) and miR-384 was detected in cells and CRC tissues by qPCR. Luteolin was found to upregulate miR-384 and downregulate PTN expressions both in CRC cells and tissues. miR-384 inhibition and PTN overexpression partially reversed the inhibition of HT-29 cells migration and invasion induced by luteolin. Target analysis revealed that miR-384 directly regulates PTN expression. The correlation analysis between PTN expression and clinical characteristics revealed that PTN expression was positively related to cancer progression. The present study demonstrated that luteolin exerts anticancer effects against CRC cells by modulating PTN via miR-384 expression suggested that PTN may serve as a promising candidate for therapeutic applications in CRC treatment.

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“…Whether SDC3-mediated regulation of MSC migration is directly linked to SDC3-mediated regulation of adhesion or via other pathways, remains to be established. In other cell types SDC3 regulates migration by functioning as a ligand for the soluble factor heparin-binding growth-associated molecule (HB-GAM) also known as pleiotrophin 43,44 . However, pleiotrophin failed to enhance migration of both wild type and Sdc3 −/− MSCs in our transwell assays, suggesting that, at least under our experimental conditions, SDC3-mediated regulation of MSC migration is not pleiotrophin-dependent.…”

Section: Discussionmentioning

confidence: 99%

MSCs from syndecan-3 null mice exhibit enhanced adhesion to collagen type I, hyperactivation of the AKT pathway and increased efficacy in inflammatory arthritis

Jones

Stefan

Kay

et al. 2020

Preprint

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1AbstractRheumatoid arthritis (RA) is a debilitating and painful inflammatory autoimmune disease characterised by the accumulation of leukocytes in the synovium, cartilage destruction and bone erosion. The immunomodulatory effects of bone marrow derived mesenchymal stem cells (MSCs) has been widely studied and the recent observations that syndecan-3 (SDC3) is selectively pro-inflammatory in the joint led us to hypothesise that SDC3 might play an important role in MSC biology. MSCs isolated from bone marrow of wild type and Sdc3−/− mice were used to assess immunophenotype, differentiation, adhesion and migration properties and cell signalling pathways. While both cell types show similar differentiation potential and forward scatter values, the cell complexity in wild type MSCs was significantly higher than in Sdc3−/− cells and was accompanied by lower spread surface area. Moreover, Sdc3−/− MSCs adhered more rapidly to collagen type I and showed a dramatic increase in AKT phosphorylation, accompanied by a decrease in ERK1/2 phosphorylation compared with control cells. In a mouse model of antigen-induced inflammatory arthritis, intraarticular injection of Sdc3−/− MSCs yielded enhanced recovery compared to injection of wild type MSCs. In conclusion, our data suggest that syndecan-3 regulates MSC adhesion and efficacy in inflammatory arthritis, likely via induction of the AKT pathway.

show abstract

Pleiotrophin and N-syndecan promote perineural invasion and tumor progression in an orthotopic mouse model of pancreatic cancer

Cited by 22 publications

References 34 publications

Syndecan-3 regulates MSC adhesion, ERK and AKT signalling in vitro and its deletion enhances MSC efficacy in a model of inflammatory arthritis in vivo

Syndecan-3 regulates MSC adhesion, ERK and AKT signalling in vitro and its deletion enhances MSC efficacy in a model of inflammatory arthritis in vivo

Luteolin suppresses colorectal cancer cell metastasis via regulation of the miR‑384/pleiotrophin axis

MSCs from syndecan-3 null mice exhibit enhanced adhesion to collagen type I, hyperactivation of the AKT pathway and increased efficacy in inflammatory arthritis

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