Cited by 96Connective Tissue Growth Factor ResearchProstate Cancer Treatment and ResearchBone and Dental Protein Studies

Involvement of Cyr61 in growth, migration, and metastasis of prostate cancer cells

Open access
Sun, Z-J, Wang, Y, Cai, Z, Chen, P-P, Tong, X-J, Xie, D·2008·British Journal of Cancer

Abstract

Cyr61 has been reported to participate in the development and progression of various cancers; however, its role in prostate cancer (PCa) still remains poorly understood. In this study, we explored the function of Cyr61 in a series of malignant PCa cell lines, including LnCap, Du145, and PC3. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and crystal violet assays demonstrated that Cyr61 was essential for the proliferation of PCa cells. Soft agar assay and xenograft analysis showed that downregulation of Cyr61 suppressed the tumorigenicity of Du145 cells both in vitro and in vivo. Either silencing the cellular Cyr61 by RNA interference or neutralising the endogenous Cyr61 by antibody inhibited the migration of Du145 cells. In contrast, purified protein of Cyr61 promoted the migration of LnCap cells in a dose-dependent manner. These results suggested that Cyr61 was involved in the migration of PCa cells. We also observed the accumulation of mature focal adhesion complexes associated with the impaired migration through Cyr61 downregulation. Also, further studies showed that Cyr61 regulated the level of activated Rac1 as well as its downstream targets, including phosphorylated JNK, E-cadherin, and p27(kip1), which are key molecules involved in cell growth, migration, and invasion. The in vivo mouse tail vein injection experiment revealed that Cyr61 affected the metastatic capacity of Du145 cells, suggesting that Cyr61 was required for prostate tumour metastasis. Altogether, our results demonstrated that Cyr61 played an important role in the tumorigenicity and metastasis of PCa cells, which will benefit the development of therapeutic strategy for PCas.

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Crossref · 10.1038/sj.bjc.6604712

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  • CCN1 stimulates cell migration in fibroblasts, smooth muscle cells, endothelial cells, and certain cancer cells.

    “Furthermore, CCN1 stimulates cell migration in fibroblasts, smooth muscle cells and endothelial cells [56,71,72], and certain cancer cells [73–75].”

    From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [74]

  • Silencing of CCN1 expression decreased tumor growth in xenografts of prostate cancer cells and pancreatic cancer cells.

    “Consistently, silencing of CCN1 expression decreased tumor growth in xenografts of prostate cancer cells [74] and pancreatic cancer cells [144].”

    From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [74]

  • CCN1 can exacerbate apoptosis of prostate cancer cells in the presence of TRAIL.

    “For example, whereas CCN1 can promote the proliferation of prostate cancer cells, CCN1 can also exacerbate apoptosis of these cells in the presence of the immune surveillance molecule TRAIL [74,76,77].”

    From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [74]

  • CCN1 can promote proliferation of prostate cancer cells.

    “For example, whereas CCN1 can promote the proliferation of prostate cancer cells, CCN1 can also exacerbate apoptosis of these cells in the presence of the immune surveillance molecule TRAIL [74,76,77].”

    From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [74]

  • Forced expression of CCN1 enhanced tumor growth in xenografts of breast cancer cells, prostate cancer cells, ovarian carcinoma cells, and squamous carcinoma cells.

    “Accordingly, subsequent studies have shown that forced expression of CCN1 enhanced tumor growth in xenografts of breast cancer cells [142], prostate cancer cells [74], ovarian carcinoma cells [78], and squamous carcinoma cells [143].”

    From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [74]

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  1. Thomas M, Finnegan CE, Rogers KM, Purcell JW, Trimble A, Johnston PG, Boland MP (2004) STAT1: a modulator of chemotherapy-induced apoptosis. Cancer Res 64: 8357–8364 15548705

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Authors
Sun, Z.-J., Wang, Y., Cai, Z., Chen, P.-P., Tong, X.-J., & Xie, D.
Affiliations
Chinese Academy of Sciences (CN)
Corresponding author
Xie, D
Venue
British Journal of Cancer
Published
2008-10-21
Volume
99
Issue
10
Pages
1656-1667
ISSN
  • 0007-0920 (ISSN-L)
  • 1532-1827
OpenAlex
W2092361248
Cited by
95
References
58
Citations by year
2025: 6 · 2024: 3 · 2023: 5 · 2022: 1 · 2021: 11 · 2020: 2 · 2019: 4 · 2018: 6 · 2017: 4 · 2016: 8 · 2015: 4 · 2014: 6 · 2013: 10 · 2012: 8
FWCI
2.33
Type
journal article
Language
en
Open access
Locations
  • British Journal of Cancer (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
  • National Natural Science Foundation of China (973 Program, 30470847, 863 Program, 30528003)
  • Chinese Academy of Sciences (KSCX-YW-R-73)
  • China Postdoctoral Science Foundation
  • Science and Technology Commission of Shanghai Municipality (05DJ14009)
  • National High-tech Research and Development Program
  • National Key Research and Development Program of China
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connective Tissue Growth Factor Research
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
  • Health Sciences › Medicine › Rheumatology › Bone and Dental Protein Studies
Keywords
CYR61, prostate cancer, cell migration, metastasis, tumorigenicity, cell proliferation, focal adhesions, Rac1 activation, JNK phosphorylation, E-cadherin, p27, tumor invasion
MeSH terms
Cell Movement, Humans, Male, Neoplasm Metastasis, Prostatic Neoplasms, Cell Line, Tumor, Cell Enlargement, Cysteine-Rich Protein 61

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