The E-F Hand Calcium-Binding Protein S100A4 Regulates the Proliferation, Survival and Differentiation Potential of Human Osteosarcoma Cells

Chen, Xian; Luther, Gaurav; Zhang, Wenwen; Guo, Nan; Wagner, Eric R.; Zhan, Lin; Wu, Ningning; Zhang, Hongmei; Wang, Ning; Wen, Sheng; He, Yong; Deng, Fang; Zhang, Junhui; Wu, Di; Zhang, Bosi; Haydon, Rex C.; Zhou, Lan; Luu, Hue H.; He, Tong‐Chuan

doi:10.1159/000354508

Cited by 44 publications

(39 citation statements)

References 65 publications

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“…Specifically, we found that IPF MPCs express higher levels of S100A4 compared with control MPCs (14). S100A4, a calcium binding protein, is upregulated in cancer stem cells, where it controls proliferation, differentiation, and metastasis (15)(16)(17)(18)(19)(20)(21)(22). S100A4 also amplifies TGF-β-induced fibroblast activation in the progressive fibrotic disorder systemic sclerosis (23).…”

Section: Introductionmentioning

confidence: 83%

“…While important, these studies are beyond the scope of the current body of work. S100A4 has also been termed metastasin because it regulates cancer cell metastasis (15)(16)(17)(18)(19)(20)(21)(22). While S100A4 levels are elevated in both cancer cells and IPF cells, IPF cells do not metastasize, suggesting that there are important differences between cancer and fibrosis in relation to S100A4 function.…”

Section: Discussionmentioning

confidence: 99%

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Calcium-binding protein S100A4 confers mesenchymal progenitor cell fibrogenicity in idiopathic pulmonary fibrosis

Xia¹,

Gilbertsen²,

Herrera³

et al. 2017

Journal of Clinical Investigation

132

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Section: Introductionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Calcium-binding protein S100A4 confers mesenchymal progenitor cell fibrogenicity in idiopathic pulmonary fibrosis

Xia¹,

Gilbertsen²,

Herrera³

et al. 2017

Journal of Clinical Investigation

132

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“…Several studies showed S100A4 to be protective against pro-apoptotic stimuli [96][97][98]. Orre et al [99] showed that S100A4 interacts with the tumor suppressor p53 in the nucleus and promotes p53 degradation.…”

Section: Wnt Signaling Target: S100a4mentioning

confidence: 99%

Underlying Mechanisms for Distant Metastasis - Molecular Biology

2017

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Concepts of MetastasisIn 1889, the English surgeon Stephen Paget illustrated his theory on metastasis with the sentence 'When a plant goes to seed, its seeds are carried in all directions, but they can only live and grow if they fall on congenial soil'. He based this 'seed and soil' hypothesis on autopsy records where he detected a discrepancy between the blood supply and frequency of metastasis in specific organs. He concluded that the development of metastasis depends on distinctive features of the tumor cells as well as the specific target organs [1,2]. This concept replaced the mechanistic hypothesis of Rudolf Virchow who considered metastasis as the arrest of tumor cell emboli in the vasculature [2]. Nowadays, metastasis is understood as a complex process of molecular and biochemical events performed by multiple actors. The concept of a 'homogenous seed' has been replaced by a heterogeneous hierarchically organized system of tumorigenic cancer stem cells and their non-tumorigenic progeny [3]. Cancer stem cells are now regarded to be the major driver in metastasis development. In addition, the idea of a sequential development of a cancer from a single primary tumor to the subsequent spread to distant sites was abandoned in the last years and replaced by a model of a simultaneous progression towards metastatic tumor disease. The currently favored model describes the evolution of systemic tumor disease as a parallel development of primary tumor and distant metastasis caused by heterogeneous tumor subpopulations [4].To understand the cellular and molecular basis of metastasis, the most acknowledged approach is the concept of the invasionmetastasis cascade proposed by Isaiah J. Fidler in 2003 and subsequently adapted by Scott Valastyan in 2011 [5,6]. The authors distinguish 6 steps in the process from primary local tumor to distant Keywords Metastasis · Molecular mechanism · Cancer therapy Summary Background:The formation of distant metastases constitutes a complex process with a variety of different genes and pathways involved. To improve patient survival, it is necessary to understand the underlying mechanisms of metastasis to allow for targeted intervention. Methods: This review provides an overview of the general concepts of metastasis, focusing on the most important genes and pathways involved and on interventional strategies. Results: Cancer cells undergo different steps to form metastasis: most prominently, local invasion, intravasation, survival in the circulation, arrest at a distant organ site and extravasation, micrometastasis formation, and metastatic colonization. In order to pass these steps, different molecular pathways are of major importance: EGF/RAS/ RAF/MEK/ERK, PI3K/Akt/mTOR, HGF/Met, Wnt/ -catenin, and VEGF signaling. The HGF/Met regulator MACC1 and the Wnt signaling target S100A4 have been shown to play a major role in the metastatic process. Each gene and pathway provides an opportunity for therapeutic intervention. Conclusion: Since metastasis represents a highly limiting factor in cancer...

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“…1, significant suppression of S100A4 expression was observed using RT-qPCR and western blotting. S100A4 is important in a variety of cellular events, including cell growth and apoptosis (18,19). However, previous discrepancy studies suggest the effect of S100A4 on cell growth and apoptosis depends on the cell type.…”

Section: Discussionmentioning

confidence: 99%

RNA interference targeting inhibition of S100A4 suppresses cell growth and promotes apoptosis in human laryngeal carcinoma Hep-2 cells

Liu

et al. 2014

Molecular Medicine Reports

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Abstract. S100A4 is a small Ca 2+ binding protein that belongs to the S100 family and is involved in a number of cellular functions, including cell cycle control, proliferation, apoptosis, and has a significant role in angiogenesis and neurite extension. However, the exact function and mechanism of S100A4 in laryngeal carcinogenesis remains to be elucidated. The present study was designed to investigate the potential use of RNA interference to inhibit S100A4 expression and activation, as well as the subsequent effect on human laryngeal cancer cell growth and apoptosis. The present study demonstrated that knockdown of S100A4 decreased the proliferation and growth of the human laryngeal cancer Hep-2 cell line. The percentages of the apoptotic cells were 4.23±1.22, 4.92±1.85 and 11.70±4.02% in the control, negative control and S100A4 short hairpin RNA (shRNA) groups, respectively, indicating significant differences among the different groups. The S100A4-mediated induction of apoptosis was demonstrated to be associated with the activation of caspase-3, caspase-8 and caspase-9. Intratumoral injection of S100A4-shRNA inhibited tumor growth in nude mice. Thus, knockdown of S100A4 inhibited the progression of laryngeal squamous carcinoma, decreased proliferation and promoted apoptosis. S100A4 is a potential candidate for therapeutic targeting of laryngeal carcinoma cells.

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The E-F Hand Calcium-Binding Protein S100A4 Regulates the Proliferation, Survival and Differentiation Potential of Human Osteosarcoma Cells

Cited by 44 publications

References 65 publications

Calcium-binding protein S100A4 confers mesenchymal progenitor cell fibrogenicity in idiopathic pulmonary fibrosis

Calcium-binding protein S100A4 confers mesenchymal progenitor cell fibrogenicity in idiopathic pulmonary fibrosis

Underlying Mechanisms for Distant Metastasis - Molecular Biology

RNA interference targeting inhibition of S100A4 suppresses cell growth and promotes apoptosis in human laryngeal carcinoma Hep-2 cells

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