S100A7 promotes the migration, invasion and metastasis of human cervical cancer cells through epithelial-mesenchymal transition

Tian, Tian; Li, Xukun; Hua, Zhen; Ma, Jin; Wu, Xiaowei; Liu, Zhihua; Chen, Hongyan; Cui, Zhonghui

doi:10.18632/oncotarget.15329

Cited by 45 publications

(45 citation statements)

References 31 publications

(46 reference statements)

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“…The phenomenon known as epithelial-mesenchymal transition (EMT) promotes invasion and metastasis in many cancers [29][30][31], and we hypothesized that S1PR1 might be involved in EMT of GC cells. We treated MGC-803 cells with 10 ng/ml TGF-β1 for 24 hours.…”

Section: S1pr1 Expression Is Elevated In a Tgf-β1 Induced Emt Modelmentioning

confidence: 99%

Galectin-1 Promotes Metastasis in Gastric Cancer Through a Sphingosine-1-Phosphate Receptor 1-Dependent Mechanism

You

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Increased expression of galectin-1 (Gal-1) in gastric cancer (GC) promotes metastasis and correlates with poor prognosis. The mechanisms by which Gal-1 promotes GC metastasis remain unknown. Methods: Gal-1and Sphingosine-1-phosphate receptor 1 (S1PR1) were determined by immunohistochemistry(IHC) and quantitative real time polymerase chain reaction (qRT-PCR) in GC specimens. Stably transfected Gal-1 or S1PR1 into SGC7901 and MGC-803 cells, western blot and invasion assays in vitro and nude mice tumorigenicity in vivo were also employed. Results: Overexpression of Gal-1 enhanced expression of S1PR1 in SGC-7901 cells, and increased cell invasion, while knockdown Gal-1 in MGC-803 cells reduced S1PR1 expression and diminished invasion. Simultaneous knockdown of Gal-1 and overexpression of S1PR1 in MGC803 cells rescued invasive ability of MGC803 cells. S1PR1 was associated with expression of epithelial-to-mesenchymal transition (EMT) markers in vitro and in clinical samples. EMT induced in MGC-803 cells by TGF-β1 was accompanied by S1PR1 activation, while knockdown of S1PR1 reduced response to TGF-β1, suggest that Gal-1 promotes GC invasion by activating EMT through a S1PR1-dependent mechanism. Overexpression of S1PR1 promoted subcutaneous xenograft growth and pulmonary metastases, and enhanced expression of EMT markers. Conclusion: Galectin-1 promotes metastasis in gastric cancer through a S1PR1- dependent mechanism, our results indicate that targeting S1PR1 may be a novel strategy to treat GC metastasis.

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Section: S1pr1 Expression Is Elevated In a Tgf-β1 Induced Emt Modelmentioning

confidence: 99%

Galectin-1 Promotes Metastasis in Gastric Cancer Through a Sphingosine-1-Phosphate Receptor 1-Dependent Mechanism

You

Wang

et al. 2018

Cell Physiol Biochem

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“…Limited studies have been done to evaluate the effect of ASCs on cervical cancer. However, one study by Tian et al found that S100A7, described above for its role in breast cancer proliferation and metastasis, has also been shown to enhance cell migration, invasion, metastasis and the epithelial to mesenchymal transition of cervical cancer . ASC secretion of two pro‐inflammatory cytokines IL‐8 and IL‐6, described below, was increased when cocultured with bladder cancer cells .…”

Section: Ascs In Cancermentioning

confidence: 99%

Adipose Stem Cells and Cancer: Concise Review

et al. 2019

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It is well established that the tumor microenvironment plays an important role in cancer development and progression. The tumor microenvironment is composed of neoplastic cells, endothelial cells, pericytes, adipocytes, fibroblasts and other connective tissue cells, extracellular matrix components, multiple stem and progenitor cells, and a diverse array of innate and adaptive immune cells [Nat Rev Cancer 2007;7:139–147]. Understanding the mechanisms behind cell–cell communication in the tumor microenvironment is critical to understanding the drivers of tumorigenesis and metastasis. In this review, we discuss the interactions between adipose stem cells, a critical component of the tumor microenvironment, and various forms of cancer. Stem Cells 2019;37:1261–1266

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“…by regulating cell proliferation, metastasis, migration, invasion, apoptosis and angiogenesis (17)(18)(19). Mechanistically, several signaling pathways have been demonstrated to have a correlation with psoriasin, including Hippo, receptor for advanced glycation endproducts (RAGE), extracellular signal-regulated kinase (ERK), β-catenin and nuclear factor (NF)-κB pathways.…”

Section: Psoriasin Overexpression Confers Drug Resistance To Cisplatimentioning

confidence: 99%

“…Similarly, psoriasin promotes cell survival by binding to c-Jun activation domain-binding protein1 and enhancing the phosphorylation of NF-κB and protein kinase B in breast cancer (20). Another study demonstrated that psoriasin binds to RAGE and activates ERK signaling to increase migration and invasion in cervical cancer (18). However, the role of psoriasin in GC and its underlying mechanisms remain unclear.…”

Section: Psoriasin Overexpression Confers Drug Resistance To Cisplatimentioning

confidence: 99%

“…Psoriasin, a low molecular weight protein (11.4 kDa), is localized in the cytoplasm, cell nucleus or secreted outside of the cell in certain cases (9,10). Dysregulated expression of psoriasin has been observed in various types of cancer, including oral squamous cell carcinoma (11), breast cancer (10,12), lung cancer (13), bladder cancer (14), skin cancer (15), head and neck cancer (16), prostate cancer (17) and cervical cancer (18). Functionally, psoriasin usually has malignant functions in cancer; however, it can also exhibit tumor suppressive effects in certain types of oral carcinoma and breast cancer by decreasing β-catenin activity (11,12).…”

Section: Introductionmentioning

confidence: 99%

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Psoriasin overexpression confers drug resistance to cisplatin by activating ERK in gastric cancer

Cui

et al. 2018

Int J Oncol

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Psoriasin, a member of the S100 multigenic family, which is aberrantly expressed in a variety of human tumors, is considered as an attractive molecular target for cancer treatment. The present study aimed to characterize the role of psoriasin in gastric cancer (GC), the associated pathways through which it contributes to cancer development and progression, and the effect of psoriasin on cellular response to pre-operative chemotherapy in patients with GC. Expression of psoriasin mRNA and protein were analyzed using quantitative polymerase chain reaction and immunohistochemistry of gastric cancer cohorts, respectively. Gastric cancer cell models with differential expression of psoriasin were generated using stable cell lines that overexpressed psoriasin. The in vitro biological functions of the cells in response to psoriasin overexpression and to chemotherapeutic agents were assessed using various cell-based assays. Psoriasin was overexpressed in patients with advanced GC, and high psoriasin levels led to poor clinical outcomes. Increasing psoriasin expression in GC cell lines promoted cell proliferation, migration and invasion in vitro. Furthermore, psoriasin overexpression caused alterations in the levels of epithelial-mesenchymal transition-associated proteins, and activated the extracellular signal-regulated kinase signaling pathway. Additionally, higher levels of psoriasin expression were significantly associated a lack of response to neoadjuvant chemotherapy in patients with GC. Psoriasin overexpression tended to decrease the sensitivity of GC cells to cisplatin, potentially by inhibiting apoptosis or increasing the S-phase population. Taken together, these results indicate that psoriasin may be a promising therapeutic target for GC treatment, and a potential molecular marker to predict patient response to pre-operative chemotherapy.

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S100A7 promotes the migration, invasion and metastasis of human cervical cancer cells through epithelial-mesenchymal transition

Cited by 45 publications

References 31 publications

Galectin-1 Promotes Metastasis in Gastric Cancer Through a Sphingosine-1-Phosphate Receptor 1-Dependent Mechanism

Galectin-1 Promotes Metastasis in Gastric Cancer Through a Sphingosine-1-Phosphate Receptor 1-Dependent Mechanism

Adipose Stem Cells and Cancer: Concise Review

Psoriasin overexpression confers drug resistance to cisplatin by activating ERK in gastric cancer

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