Pigment Epithelium-Derived Factor Promotes the Growth and Migration of Human Esophageal Squamous Cell Carcinoma

Tang, Derong; Li, Chenglin; Xu, Kan; Wu, Qingquan; Qi-you, Chen; Liu, Jun-Jie; Ji, Jian; Zang, Bao; Chen, Chen; Gu, Biao; Zhao, Jianqiang

doi:10.3389/fonc.2019.01520

Cited by 8 publications

(8 citation statements)

References 33 publications

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“…Although PEDF has been shown to play a vital role in the metastasis of many types of tumors, there are few reports on how PEDF affects the progression of ESCC. Tang et al previously reported that PEDF could promote esophageal tumor cell proliferation and apoptosis (27). In their study, they found that PEDF is overexpressed in esophageal carcinoma tissues and cells.…”

Section: Discussionmentioning

confidence: 83%

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Upregulation of PEDF Predicts a Poor Prognosis and Promotes Esophageal Squamous Cell Carcinoma Progression by Modulating the MAPK/ERK Signaling Pathway

et al. 2021

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Invasion and metastasis represent the primary causes of therapeutic failure in patients diagnosed with esophageal squamous cell carcinoma (ESCC). The lack of effective treatment strategies for metastatic ESCC is the major cause of the low survival rate. Therefore, it is crucial to understand the molecular mechanisms underlying ESCC metastasis and identify potential biomarkers for targeted therapy. Herein, we reported that PEDF is significantly correlated with tumor cell invasion and metastasis in ESCC. The high expression of PEDF is an independent unfavorable prognostic factor for ESCC patients’ overall survival (OS). We successfully developed and verified a nomogram to predict the preoperative OS of ESCC patients, and the actual and nomogram-predicted 1-, 3-, and 5-year survival rates had good consistency. The receiver operating characteristic (ROC) curve showed that the area under the curve (AUC) values for 1-, 3- and 5- survival were 0.764, 0.871, and 0.91, respectively. Overexpression of PEDF significantly promoted the migration and invasion of ESCC cells in vitro, while silencing PEDF yielded the opposite effects. Elevated levels of PEDF altered the expression of proteins involved in epithelial–mesenchymal transition (EMT), as indicated by the upregulation of N-cadherin and the downregulation of α-catenin and E-cadherin in ESCC cells. Mechanistically, PEDF promoted tumor cell motility and EMT by activating the MAPK/ERK signaling pathway. In conclusion, our results reveal that PEDF is involved in ESCC metastasis and could act as a prognostic factor for ESCC. Our research provides a fresh perspective into the mechanism of ESCC metastasis.

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Section: Discussionmentioning

confidence: 83%

“…PEDF is also significantly associated with hepatocellular carcinoma progression and metastasis (26). Recently, Tang et al reported that PEDF promotes esophageal cancer cell growth (27). However, the molecular mechanism by which PEDF functions in the tumorigenesis and clinical progression of ESCC remains elusive.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of PEDF Predicts a Poor Prognosis and Promotes Esophageal Squamous Cell Carcinoma Progression by Modulating the MAPK/ERK Signaling Pathway

et al. 2021

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“…For example, SERPINF1 showed anti-tumor effects by inhibiting angiogenesis in melanoma, cholangiocarcinoma, and breast cancer [ 11 , 29 , 30 ]. However, many studies substantiated that SERPINF1 promotes the growth and metastasis of esophageal cancer, liver cancer, and ovarian cancer [ 12 , 13 , 31 ]. Li et al reported that SERPINF1 exhibits contrasting intracellular and extracellular functions in hepatocellular carcinoma [ 14 ].…”

Section: Discussionmentioning

confidence: 99%

“…Serpin family F member 1 (SERPINF1), also known as pigment epithelium-derived factor (PEDF), is a multifunctional secreted protein [ 9 ] that can exert an anti-tumor effect by inhibiting angiogenesis [ 10 , 11 ]. Interestingly, it has also been documented to promote the proliferation and invasion of tumor cells [ 12 , 13 ]. In this respect, Li et al reported that SERPINF1 exhibits contrasting intracellular and extracellular functions in hepatocellular carcinoma [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

SERPINF1 Mediates Tumor Progression and Stemness in Glioma

Song

Huo

et al. 2023

Genes

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Serpin family F member 1 (SERPINF1) reportedly plays multiple roles in various tumors; however, its clinical significance and molecular functions in glioma have been largely understudied. In the present study, we analyzed the prognostic value of SERPINF1 in three independent glioma datasets. Next, we explored the molecular functions and transcriptional regulation of SERPINF1 at the single-cell level. Moreover, in vitro experiments were conducted to evaluate the roles of SERPINF1 in the proliferation, invasion, migration, and stemness of glioma cells. Our results showed that a higher expression of SERPINF1 correlated with a poor overall survival rate in glioma patients (hazard ratio: 4.061 in TCGA, 2.017 in CGGA, and 1.675 in GSE16011, p < 0.001). Besides, SERPINF1 knockdown could suppress the proliferation, invasion, and migration of glioma cells in vitro. In addition, SERPINF1 expression was significantly upregulated in glioma stem cells (GSCs) compared to parental glioma cells. Knocking down SERPINF1 impaired the sphere formation of GSC-A172 and GSC-LN18. Bioinformatics analysis revealed that Notch signaling activation was closely associated with high SERPINF1 expression at the single-cell level. Furthermore, STAT1, CREM, and NR2F2 may participate in the transcriptional regulation of SERPINF1 in glioma. Overall, our results suggest that SERPINF1 may be a candidate prognostic predictor and potential therapeutic target for glioma.

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“…58 LDLR, RBP4, and PEDF are known to promote tumor growth, proliferation, and migration. [59][60][61] IGF is a mitogen and is involved in regulating cell proliferation, apoptosis, and transformation by interacting with the IGF-I receptor. 62 The mitogenic effect of IGF on cancer cells is determined by bioavailability and interaction with IGF-IR, which IGFBPs regulate.…”

Section: Protein-protein Interactions and Pathways Analysismentioning

confidence: 99%

Effect of nonsteroidal anti‐inflammatory drugs (aspirin and naproxen) on inflammation‐associated proteomic profiles in mouse plasma and prostate during TMPRSS2‐ERG (fusion)‐driven prostate carcinogenesis

Prasad,

Mishra,

Kant

et al. 2024

Molecular Carcinogenesis

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Recent preclinical studies have shown that the intake of nonsteroidal anti‐inflammatory drugs (NSAIDs) aspirin and naproxen could be an effective intervention strategy against TMPRSS2‐ERG fusion‐driven prostate tumorigenesis. Herein, as a follow‐up mechanistic study, employing TMPRSS2‐ERG (fusion) positive tumors and plasma from TMPRSS2‐ERG. Ptenflox/flox mice, we profiled the stage specific proteomic changes (focused on inflammatory circulating and prostate tissue/tumor‐specific cytokines, chemokines, and growth factors/growth signaling‐associated molecules) that contribute to prostate cancer (PCa) growth and progression in the TMPRSS2‐ERG fusion‐driven mouse model of tumorigenesis. In addition, the association of the protective effects of NSAIDs (aspirin 1400 ppm and naproxen 400 ppm) with the modulation of these specific molecular pathways was determined. A sandwich Elisa based membrane array‐proteome profiler identifying 111 distinct signaling molecules was employed. Overall, the plasma and prostate tissue sample analyses identified 54 significant and differentially expressed cytokines, chemokines, and growth factors/growth signaling‐associated molecules between PCa afflicted mice (TMPRSS2‐ERG. Ptenflox/flox, age‐matched noncancerous controls, NSAIDs‐supplemented and no‐drug controls). Bioinformatic analysis of the array outcomes indicated that the protective effect of NSAIDs was associated with reduced expression of (a) tumor promoting inflammatory molecules (M‐CSF, IL‐33, CCL22, CCL12, CX3CL1, CHI3L1, and CD93), (b) growth factors‐ growth signaling‐associated molecules (Chemerin, FGF acidic, Flt‐3 ligand, IGFBP‐5, and PEDF), and (c) tumor microenvironment/stromal remodeling proteins MMP2 and MMP9. Overall, our findings corroborate the pathological findings that protective effects of NSAIDs in TMPSS2‐ERG fusion‐driven prostate tumorigenesis are associated with antiproliferative and anti‐inflammatory effects and possible modulation of the immune cell enriched microenvironment.

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Pigment Epithelium-Derived Factor Promotes the Growth and Migration of Human Esophageal Squamous Cell Carcinoma

Cited by 8 publications

References 33 publications

Upregulation of PEDF Predicts a Poor Prognosis and Promotes Esophageal Squamous Cell Carcinoma Progression by Modulating the MAPK/ERK Signaling Pathway

Upregulation of PEDF Predicts a Poor Prognosis and Promotes Esophageal Squamous Cell Carcinoma Progression by Modulating the MAPK/ERK Signaling Pathway

SERPINF1 Mediates Tumor Progression and Stemness in Glioma

Effect of nonsteroidal anti‐inflammatory drugs (aspirin and naproxen) on inflammation‐associated proteomic profiles in mouse plasma and prostate during TMPRSS2‐ERG (fusion)‐driven prostate carcinogenesis

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