Stem Cell Associated Genes Working with One MiRNA Cluster Have Different Clinic Pathologic Values in Gastric Cancer

Wu, Qiong; Yang, Zhiping; Hu, Songhua; Su, Tao; An, Yanxin; Zhang, Zhiyong; Nie, Yongzhan; Wang, Xin; Shi, Yongquan; Fan, Daiming

doi:10.1007/s12253-011-9407-6

Cited by 2 publications

(3 citation statements)

References 26 publications

(28 reference statements)

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“…Our observations are in line with recent reports showing that CD248-deficient fibroblasts or pericytes also have defects in migration and proliferation that may [14,61] or may not [49] depend on PDGF-BB. The apparent discordant findings in the literature likely reflect differences in experimental approaches.…”

Section: Discussionsupporting

confidence: 93%

“…The apparent discordant findings in the literature likely reflect differences in experimental approaches. Studies by Tomkowicz et al suggest that CD248 may recruit Src/PI-3 Kinase and cFos pathways to enhance PDGF-BB-induced signals emanating from the PDGF-receptor [61]. Further study will be necessary to elucidate the intracellular pathways responsible for the reduced PDGF-BB induced CD248 CyD/CyD fibroblast migration.…”

Section: Discussionmentioning

confidence: 99%

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CD248 facilitates tumor growth via its cytoplasmic domain

et al. 2011

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BackgroundStromal fibroblasts participate in the development of a permissive environment for tumor growth, yet molecular pathways to therapeutically target fibroblasts are poorly defined. CD248, also known as endosialin or tumor endothelial marker 1 (TEM1), is a transmembrane glycoprotein expressed on activated fibroblasts. We recently showed that the cytoplasmic domain of CD248 is important in facilitating an inflammatory response in a mouse model of arthritis. Others have reported that CD248 gene inactivation in mice results in dampened tumor growth. We hypothesized that the conserved cytoplasmic domain of CD248 is important in regulating tumor growth.MethodsMice lacking the cytoplasmic domain of CD248 (CD248CyD/CyD) were generated and evaluated in tumor models, comparing the findings with wild-type mice (CD248WT/WT).ResultsAs compared to the response in CD248WT/WT mice, growth of T241 fibrosarcomas and Lewis lung carcinomas was significantly reduced in CD248CyD/CyD mice. Tumor size was similar to that seen with CD248-deficient mice. Conditioned media from CD248CyD/CyD fibroblasts were less effective at supporting T241 fibrosarcoma cell survival. In addition to our previous observation of reduced release of activated matrix metalloproteinase (MMP)-9, CD248CyD/CyD fibroblasts also had impaired PDGF-BB-induced migration and expressed higher transcripts of tumor suppressor factors, transgelin (SM22α), Hes and Hey1.ConclusionsThe multiple pathways regulated by the cytoplasmic domain of CD248 highlight its potential as a therapeutic target to treat cancer.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

CD248 facilitates tumor growth via its cytoplasmic domain

et al. 2011

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“…CSCs are defined as a small side population (SP) of cancer cells, with the capability of both self-renewal and pluripotency[2], mediating tumor initiation, metastasis, recurrence and drug resistance[3],[4]. To date, the possible existence of CSCs has been identified in leukemia[5],[6], breast cancers[7],[8] and other solid malignancies[6],[9]-[11].…”

Section: Introductionmentioning

confidence: 99%

Sox2 enhances the tumorigenicity and chemoresistance of cancer stem-like cells derived from gastric cancer

et al. 2012

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Gastric cancer stem-like cells (GCSCs) have been identified to possess the ability of self-renewal and tumor initiation. However, the mechanisms involved remain largely unknown. Here, we isolated and characterized the GCSCs by side population (SP) sorting procedure and cultured sphere cells (SC) from human gastric cancer cell lines SGC-7901, BGC-823, MGC-803, HGC-27 and MKN-28. The sorting and culture assay revealed that SP cells proliferated in an asymmetric division manner. In addition, SP cells exhibited a higher potential of spheroid colony formation and greater drug resistance than non-SP cells (NSP). Moreover, the SC were found with enhanced capabilities of drug resistance in vitro and tumorigenicity in vivo. Sox2 mRNA and protein was highly and significantly overexpressed in the SP cells and SC. Importantly, downregulation of Sox2 with siRNA obviously reduced spheroid colony formation and doxorubicin efflux, as well as increased apoptosis rate in sphere cells in vitro and suppressed tumorigenicity in vivo. These results suggest that both SP cells and cultured SC enrich with GCSCs and that Sox2 plays a pivotal role in sustaining stem cell properties and might be a potential target for gastric cancer therapy.

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Stem Cell Associated Genes Working with One MiRNA Cluster Have Different Clinic Pathologic Values in Gastric Cancer

Cited by 2 publications

References 26 publications

CD248 facilitates tumor growth via its cytoplasmic domain

CD248 facilitates tumor growth via its cytoplasmic domain

Sox2 enhances the tumorigenicity and chemoresistance of cancer stem-like cells derived from gastric cancer

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