HSP27 mediates SPARC‐induced changes in glioma morphology, migration, and invasion

Golembieski, William; Thomas, Stacey L.; Schultz, Chad R.; Yunker, Christopher K.; McClung, Heather; Lemke, Nancy; Cazacu, Simona; Barker, Thomas H.; Sage, E. Helene; Brodie, Chaya; Rempel, Sandra A.

doi:10.1002/glia.20679

Cited by 61 publications

(88 citation statements)

References 41 publications

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“…4A) HSP27 has also been implicated in SPARC-related migration and invasion of glioma cells. 32 In our analysis, there was a significant positive correlation (Pearson's coefficient; p = 0.009) between stromal SPARC level and CRC HSP27 (Fig. 5) but not between CRC SPARC and CRC HSP27.…”

Section: Resultsmentioning

confidence: 48%

“…30,31 HSP27, one of the smallest HSPs, has been associated with clinical outcomes in different solid tumors, including a positive correlation with SPARC in gliomas. 32 In our study, IHC analysis demonstrated that HSP27 expression in CRC was proportionately correlated with expression of SPARC in stromal cells but not in SPARC cancer cells. These findings supported potential functional roles of stromal SPARC on HSP27 expression.…”

Section: Discussionmentioning

confidence: 44%

“…There was no correlation of cancer cell SPARC to HSP27 expression suggesting that there are different regulatory roles of SPARC in the cancer cells and its microenvironment. Elevated HSP27 in cells has been shown to regulate cell contraction, migration and shape which are essential events that tumor cells undergo during progression 32 and, in CRC, HSP27 has also been demonstrated as an independent prognostic factor. 37 Although the mechanisms governing SPARC, VEGF-A and HSP27 need further assessment, our results strongly indicate that stromal SPARC level is much more influential than tumor SPARC level in regulating factors associated with LVI tumor progression.…”

Section: Discussionmentioning

confidence: 99%

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Lymphovascular invasion of colorectal cancer is correlated to SPARC expression in the tumor stromal microenvironment

Yoshimura

Nagahara²,

Kuo³

et al. 2011

Epigenetics

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Section: Resultsmentioning

confidence: 48%

Section: Discussionmentioning

confidence: 44%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Lymphovascular invasion of colorectal cancer is correlated to SPARC expression in the tumor stromal microenvironment

Yoshimura

Nagahara²,

Kuo³

et al. 2011

Epigenetics

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“…Similarly, controversy over the role of SPARC was also evident in carcinoma of breast and skin, where both oncogenic and tumor-suppressive roles were observed in multiple in vitro, in vivo, and clinical studies (50). On the other hand, the tumorand metastasis-suppressive role of SPARC has been well documented for gastrointestinal, ovarian, pancreatic, and colon cancers, whereas the oncogenic role was verified in glioma (38,(51)(52)(53)(54)(55). Therefore, the role of SPARC in tumor progression appears to be complex and specific to the tissue type and stages of the disease.…”

Section: Discussionmentioning

confidence: 99%

Secreted Protein Acidic and Rich in Cysteine (SPARC) Mediates Metastatic Dormancy of Prostate Cancer in Bone

Sharma

Xing

Yin

et al. 2016

Journal of Biological Chemistry

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Prostate cancer is known to frequently recur in bone; however, how dormant cells switch its phenotype leading to recurrent tumor remains poorly understood. We have isolated two syngeneic cell lines (indolent and aggressive) through in vivo selection by implanting PC3mm stem-like cells into tibial bones. We found that indolent cells retained the dormant phenotype, whereas aggressive cells grew rapidly in bone in vivo, and the growth rates of both cells in culture were similar, suggesting a role of the tumor microenvironment in the regulation of dormancy and recurrence. Indolent cells were found to secrete a high level of secreted protein acidic and rich in cysteine (SPARC), which significantly stimulated the expression of BMP7 in bone marrow stromal cells. The secreted BMP7 then kept cancer cells in a dormant state by inducing senescence, reducing "stemness," and activating dormancy-associated p38 MAPK signaling and p21 expression in cancer cells. Importantly, we found that SPARC was epigenetically silenced in aggressive cells by promoter methylation, but 5-azacytidine treatment reactivated the expression. Furthermore, high SPARC promoter methylation negatively correlated with disease-free survival of prostate cancer patients. We also found that the COX2 inhibitor NS398 down-regulated DNMTs and increased expression of SPARC, which led to tumor growth suppression in bone in vivo. These findings suggest that SPARC plays a key role in maintaining the dormancy of prostate cancer cells in the bone microenvironment.

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“…13,[18][19][20][21] To confirm that the TGF-b1-induced migration of hPDL cells is dependent on Hsp27, Hsp27-specific antibody was used. We also found that TGF-b1-induced migration was significantly inhibited by Hsp27 antibody treatment (Fig.…”

Section: Tgf-b B1 Increased Migration Of Hpdl Cellsmentioning

confidence: 99%

Transforming Growth Factor .BETA.1 Promotes Migration of Human Periodontal Ligament Cells through Heat Shock Protein 27 Phosphorylation

Kwon

Kim

Fujii

et al. 2011

Biological & Pharmaceutical Bulletin

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The human periodontal ligament (hPDL) is a highly specialized connective tissue located between the tooth root and alveolar bone. Once the hPDL is severely damaged by periodontal disease, its regeneration is known to be difficult. 1) hPDL cells can serve as an in vitro model to determine the effects of growth factors implicated in periodontal repair or regeneration. Cell migration generally plays roles in tissue formation and wound healing as tissue repair takes place following an injury, which involves the processes of inflammation, new tissue formation, and scar formation.2,3) The migration of hPDL cells is also a critical function in the initiation of periodontal wound healing. 2,4) Transforming growth factor b1 (TGF-b1) is a multifunctional peptide that regulates various cellular activities, including proliferation, differentiation, and expression of extracellular matrix proteins.5) TGF-b1 is a potent modulator of tissue repair in various tissues. It was reported that TGF-b1 alone or in combination with other growth factors accelerates various phases of wound healing.6,7) TGF-b1 may also play an important role in the modulation of tissue formation and development of the periodontium.8) The addition of TGF-b1 to gingival and periodontal ligament fibroblast cell cultures was shown to enhance RNA and protein synthesis. 9)Heat shock protein 27 (Hsp27) acts as ATP-independent molecular chaperone.10) In addition to its chaperone function, Hsp27 also seems to be an important regulator of structural integrity and membrane stability, actin polymerization and intermediate filament cytoskeleton formation, cell migration, epithelial cell-cell adhesion, cell cycle progression, proinflammatory gene expression, signal transduction pathways, mRNA stabilization, differentiation, and apoptosis.11,12) Previous results strongly suggested that phosphorylated Hsp27 was critically involved in the migration process, possibly through the association with signal transducer and activator of transcription 3 (STAT3) and focal adhesion kinase (FAK).13) Cell migration is regulated by various signaling pathway including the b1 integrin, Akt, extracellular signalregulated kinase (ERK) and nuclear factor-kappaB-dependent pathways through TGF-b1 in human cancer cells.14,15) In our previous study, we confirmed that TGF-b1-induced Hsp27 activation promotes the migration of mouse dental papilla-derived MDPC-23 cells.16) Dentinal healing and repair are the result of successive and interrelated processes that include proliferation, chemotaxis, and differentiation of dental pulp cells into odontoblasts, leading to reparative dentin formation. 17) However, the underlying mechanism of TGF-b1 responsible for regulating hPDL cell migration has not been fully elucidated. Because hPDL cells are responsible for tissue regeneration and mineralized tissue matrix formation, and cell migration are critical processes in tissue regeneration, it is valuable to clarify the precise mechanism of the cell migration of hPDL cells. In this study, we therefore investig...

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HSP27 mediates SPARC‐induced changes in glioma morphology, migration, and invasion

Cited by 61 publications

References 41 publications

Lymphovascular invasion of colorectal cancer is correlated to SPARC expression in the tumor stromal microenvironment

Lymphovascular invasion of colorectal cancer is correlated to SPARC expression in the tumor stromal microenvironment

Secreted Protein Acidic and Rich in Cysteine (SPARC) Mediates Metastatic Dormancy of Prostate Cancer in Bone

Transforming Growth Factor .BETA.1 Promotes Migration of Human Periodontal Ligament Cells through Heat Shock Protein 27 Phosphorylation

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