Calprotectin induces cell death in human prostate cancer cell (LNCaP) through survivin protein alteration

Sattari, Mina; Pazhang, Yaghub; Imani, Mehdi

doi:10.1002/cbin.10328

Cited by 8 publications

(4 citation statements)

References 46 publications

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“…Consistent with a role in epithelial maturation and renewal, S100A8/A9 induces autophagy and apoptosis (Ghavami et al 2004; Ghavami et al 2008) and significantly increases caspase 3/caspase 7 activity in multiple human cell types (Ghavami et al 2010). In prostate carcinoma cells, calprotectin appears to induce cell death by downregulating the antiapoptotic protein survivin and increasing reactive-oxygen species (Sattari et al 2014). S100A9 alone promoted apoptosis and compromised growth of acute promyelocytic leukemia cells (Zhu et al 2017).…”

Section: Role Of Calprotectin In Cellular Functionsmentioning

confidence: 99%

Calprotectin and the Initiation and Progression of Head and Neck Cancer

et al. 2018

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Calprotectin (S100A8/A9), a heterodimeric complex of calcium-binding proteins S100A8 and S100A9, is encoded by genes mapping to the chromosomal locus 1q21.3 of the epidermal differentiation complex. Whereas extracellular calprotectin shows proinflammatory and antimicrobial properties by signaling through RAGE and TLR4, intracytoplasmic S100A8/A9 appears to be important for cellular development, maintenance, and survival. S100A8/A9 is constitutively expressed in myeloid cells and the stratified mucosal epithelia lining the oropharyngeal and genitourinary mucosae. While upregulated in adenocarcinomas and other cancers, calprotectin mRNA and protein levels decline in head and neck squamous cell carcinoma (HNSCC). S100A8/A9 is also lost during head and neck preneoplasia (dysplasia). Calprotectin decrease does not correlate with the clinical stage (TNM) of HNSCC. When expressed in carcinoma cells, S100A8/A9 downregulates matrix metalloproteinase 2 expression and inhibits invasion and migration in vitro. S100A8/A9 regulates cell cycle progression and decelerates cancer cell proliferation by arresting at the G2/M checkpoint in a protein phosphatase 2α-dependent manner. In HNSCC, S100A8 and S100A9 coregulate with gene networks controlling cellular development and differentiation, cell-to-cell signaling, and cell morphology, while S100A8/A9 appears to downregulate expression of invasion- and tumorigenesis-associated genes. Indeed, tumor formation capacity is attenuated in S100A8/A9-expressing carcinoma cells in vivo. Hence, intracellular calprotectin appears to function as a tumor suppressor in head and neck carcinogenesis. When compared with S100A8/A9-low HNSCC based on analysis of TCGA, S100A8/A9-high HNSCC shows significant upregulation of apoptosis-related genes, including multiple caspases. Accordingly, S100A8/A9 facilitates DNA damage responses in HNSCC, promotes apoptotic cell death, and confers sensitivity to cisplatin and X-radiation in vitro. In the tumor milieu, loss of S100A8/A9 strongly associates with poor squamous differentiation and higher tumor grading, EGFR upregulation, increased DNA methylation, and, finally, poorer overall survival for patients with HNSCC. Hence, intracellular calprotectin shows a multifaceted protective role against the development of HNSCC.

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Section: Role Of Calprotectin In Cellular Functionsmentioning

confidence: 99%

Calprotectin and the Initiation and Progression of Head and Neck Cancer

et al. 2018

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“…Survivin localizes in the mitochondria and inhibits apoptosis. Reports indicate that Survivin protects cancer cells from drug-induced cell death [35]. Many studies indicated that aberrant expression of Survivin is associated with poor prognosis and drug/radiation resistance in breast cancers [36][37][38].…”

Section: Discussionmentioning

confidence: 99%

Ajuba Overexpression Promotes Breast Cancer Chemoresistance and Glucose Uptake through TAZ‐GLUT3/Survivin Pathway

Zhao

et al. 2022

BioMed Research International

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The LIM protein Ajuba has been implicated in the development of human cancers. To date, its expression pattern and biological significance in breast cancers (BC) have not been fully investigated. In the current study, we examined Ajuba protein levels in 93 invasive ductal carcinoma specimens by immunohistochemistry. The Ajuba expression level was elevated in breast cancer tissue compared with normal tissue. Ajuba overexpression is correlated with advanced tumor-node-metastasis (TNM) stage, positive node status, and adverse patient outcomes. The Ajuba protein level was also higher in BC cell lines compared to normal breast epithelial cell line MCF-10A. Ectopically expressed Ajuba in MCF-7 cells stimulated in vitro and in vivo cell growth, invasion, cell cycle progression, and decreased paclitaxel-induced apoptosis. RNA-sequencing (RNA-seq) followed by gene set enrichment analysis (GSEA) analysis showed that Ajuba overexpression regulated the Hippo signaling pathway. Ajuba overexpression also increased glucose uptake and increased expression of TAZ, GLUT3, and Survivin. TAZ knockdown abolished the role of Ajuba on GLUT3 and Survivin induction. The ChIP assay showed that TEAD4, a major TAZ binding transcription factor, could bind to the GLUT3 and Survivin promoter regions. In conclusion, our data demonstrated that elevated Ajuba expression is correlated with poor BC prognosis and regulated malignant behavior through TAZ-GLUT3/Survivin signaling in BC cells.

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“…23 , 24 Previous studies indicated that Survivin could maintain mitochondrial function and protect cancer cell from cell death induced by chemotherapeutic drugs. 25 Survivin expression indicates worse prognosis in patients with bladder cancer. 26 Survivin has also been reported to be crucial for the development of chemoresistance in bladder cancer.…”

Section: Discussionmentioning

confidence: 99%

AATF is Overexpressed in Human Bladder Cancer and Regulates Chemo-Sensitivity Through Survivin

Tan¹,

Fu²,

Dong³

2021

OTT

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Objective Dysregulation of apoptosis antagonizing transcription factor (AATF) has been reported to be closely associated with human cancers. However, its involvement in human bladder cancer (BC) remains unexplored. This study aimed to investigate the clinical significance and biological roles of AATF in human bladder cancers. Methods AATF protein expression was examined in 107 cases of bladder cancer tissues using immunohistochemistry. AATF plasmid transfection and small interfering RNA (siRNA) knockdown were performed in T24 and 5637 cell lines. CCK-8, colony formation, annexin V/PI, JC-1 staining, and Western blotting were carried out to investigate the biological roles and underlying mechanisms of AATF in bladder cancer cells. Results Our results showed that AATF expression was upregulated in human bladder cancer specimens and correlated with T stage. Analysis of the Oncomine database showed elevation of AATF mRNA in BC tissues. The Cancer Genome Atlas (TCGA) data suggested that high AATF expression correlated with poor patient survival. Western blotting showed that AATF protein expression was higher in BC cell lines compared to normal bladder transitional epithelial cell line SV-HUC-1. CCK-8 and colony assays showed that ectopic AATF expression upregulated cell growth rate and colony numbers. CCK-8, annexin V/propidium iodide (PI), JC-1 assays and Western blotting showed that AATF overexpression decreased cisplatin sensitivity, downregulated cisplatin-induced apoptosis and upregulated mitochondrial membrane potential, with decreased cytochrome c and cleaved-PARP expression. AATF siRNA knockdown showed the opposite effects. Mechanistically, AATF overexpression upregulated cyclin E and Survivin at both mRNA and protein levels. The decreased cisplatin sensitivity/apoptosis induced by ectopic AATF were reversed after treatment with Survivin inhibitor YM155. Conclusion Our results showed that AATF was overexpressed in human bladder cancers and promoted malignant behavior by regulating cyclin E and Survivin, indicating AATF could serve as a malignant biomarker and potential therapeutic target in BC.

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Calprotectin induces cell death in human prostate cancer cell (LNCaP) through survivin protein alteration

Cited by 8 publications

References 46 publications

Calprotectin and the Initiation and Progression of Head and Neck Cancer

Calprotectin and the Initiation and Progression of Head and Neck Cancer

Ajuba Overexpression Promotes Breast Cancer Chemoresistance and Glucose Uptake through TAZ‐GLUT3/Survivin Pathway

AATF is Overexpressed in Human Bladder Cancer and Regulates Chemo-Sensitivity Through Survivin

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