scholarly journals Downregulation of Fibronectin 1 Attenuates ATRA-induced Inhibition of Cell Migration and Invasion in Neuroblastoma Cells

2021 ◽  
Author(s):  
Xiaolin Tan ◽  
Wei Gong ◽  
Bo Chen ◽  
Baocheng Gong ◽  
Zhongyan Hua ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Migration ◽  
Retinoic Acid ◽  
Neuroblastoma Cells ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Protein Protein Interaction ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Related Pathway

Abstract Neuroblastoma (NB) is the most common malignant extra cranial solid tumors in children. It has been well established that retinoic acid (RA) inhibits proliferation of neuroblastoma (NB) by blocking cells at G1 phase of the cell cycle. Clinically, RA has been successfully used to treat NB patients. However, the precise mechanism underlying the potent action of RA-treated NB is not fully explored. In this work, we carried out a gene expression profiling by RNA sequencing on all-trans retinoic acid (ATRA)-treated NB cells. Cancer-related pathway enrichment and subsequent protein-protein interaction (PPI) network analysis identified Fibronectin 1 (FN1) as one of the central molecules in the network, which was significantly upregulated during ATRA treatment.In addition, we found that although downregulation of FN1 had no significant effects on either cell proliferation or cell cycle distributions in the presence or absence of ATRA, it increased cell migration and invasion in NB cells and partially blocked ATRA-induced inhibition of cell migration and invasion in SY5Y NB cells. Consistent with this finding, FN1 expression levels in NB patients positively correlate with their overall survivals. Taken together, our data suggest that FN1 is a potential target for effective ATRA treatment on NB patients, likely by facilitating ATRA-induced inhibition of cell migration and invasion.

Novel azolyl-(phenylmethyl)]aryl/heteroarylamines: Potent CYP26 inhibitors and enhancers of all-trans retinoic acid activity in neuroblastoma cells

2008 ◽  
Vol 16 (17) ◽  
pp. 8301-8313 ◽  
Author(s):  
Mohamed Sayed Gomaa ◽  
Jane L. Armstrong ◽  
Beatrice Bobillon ◽  
Gareth J. Veal ◽  
Andrea Brancale ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Neuroblastoma Cells ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

scholarly journals All-Trans Retinoic Acid Enhances Matrix Metalloproteinase 2 Expression and Secretion in Human Myeloid Leukemia THP-1 Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Hien Thi Vu ◽  
Thi Xoan Hoang ◽  
Jae Young Kim
Keyword(s):  
Retinoic Acid ◽  
Matrix Metalloproteinase ◽  
Calcium Ion ◽  
Myeloid Leukemia ◽  
Leukemia Cell Line ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

All-trans retinoic acid (ATRA) is an effective drug for the induction therapy of acute promyelocytic leukemia. However, the treatment is associated with adverse events such as retinoic acid syndrome (RAS) in some patients, whose histologic characteristics included organ infiltration by leukemic cells. Matrix metalloproteinase 2 (MMP-2) is often upregulated in tumor cells and plays a role in tumor cell migration and invasion by degrading the extracellular matrix. In this study, we examined the possible modulatory effects of ATRA on MMP-2 expression and secretion in human myeloid leukemia cell line THP-1. The cells were treated with various concentrations of ATRA, and MMP-2 expression and secretion were examined. MMP-2 expression and secretion started to increase with ATRA concentration as low as 0.1 nM and gradually increased thereafter. Agonists of retinoic acid receptor (RAR) or retinoid X receptor (RXR) alone could enhance MMP-2 secretion, and RAR or RXR antagonists alone could reverse ATRA-induced MMP-2 secretion. ATRA increased intracellular calcium ion levels, and a calcium-channel blocker inhibited ATRA-induced MMP-2 secretion. Dexamethasone suppressed ATRA-induced MMP-2 secretion. Our results suggest that ATRA enhances MMP-2 expression and secretion in human myeloid leukemia THP-1 cells in a calcium ion dependent manner through RAR/RXR signaling pathways, and this enhanced expression and secretion may be associated with the possible mechanisms of RAS.

scholarly journals Caspases uncouple p27Kip1 from cell cycle regulated degradation and abolish its ability to stimulate cell migration and invasion

Oncogene ◽  
2016 ◽  
Vol 35 (35) ◽  
pp. 4580-4590 ◽  
Author(s):  
S R Podmirseg ◽  
H Jäkel ◽  
G D Ranches ◽  
M K Kullmann ◽  
B Sohm ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Migration ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Stimulate Cell

scholarly journals Broussoflavonol B from Broussonetia kazinoki Siebold Exerts Anti-Pancreatic Cancer Activity through Downregulating FoxM1

Molecules ◽  
2020 ◽  
Vol 25 (10) ◽  
pp. 2328
Author(s):  
Ji Hye Jeong ◽  
Jae-Ha Ryu
Keyword(s):  
Cell Cycle ◽  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Cellular Proliferation ◽  
Cyclin B1 ◽  
Human Pancreatic Cancer ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Cancer Activity

Pancreatic cancer has a high mortality rate due to poor rates of early diagnosis. One tumor suppressor gene in particular, p53, is frequently mutated in pancreatic cancer, and mutations in p53 can inactivate normal wild type p53 activity and increase expression of transcription factor forkhead box M1 (FoxM1). Overexpression of FoxM1 accelerates cellular proliferation and cancer progression. Therefore, inhibition of FoxM1 represents a therapeutic strategy for treating pancreatic cancer. Broussoflavonol B (BF-B), isolated from the stem bark of Broussonetia kazinoki Siebold has previously been shown to inhibit the growth of breast cancer cells. This study aimed to investigate whether BF-B exhibits anti-pancreatic cancer activity and if so, identify the underlying mechanism. BF-B reduced cell proliferation, induced cell cycle arrest, and inhibited cell migration and invasion of human pancreatic cancer PANC-1 cells (p53 mutated). Interestingly, BF-B down-regulated FoxM1 expression at both the mRNA and protein level. It also suppressed the expression of FoxM1 downstream target genes, such as cyclin D1, cyclin B1, and survivin. Cell cycle analysis showed that BF-B induced the arrest of G0/G1 phase. BF-B reduced the phosphorylation of extracellular signal-regulated kinase ½ (ERK½) and expression of ERK½ downstream effector c-Myc, which regulates cell proliferation. Furthermore, BF-B inhibited cell migration and invasion, which are downstream functional properties of FoxM1. These results suggested that BF-B could repress pancreatic cancer cell proliferation by inactivation of the ERK/c-Myc/FoxM1 signaling pathway. Broussoflavonol B from Broussonetia kazinoki Siebold may represent a novel chemo-therapeutic agent for pancreatic cancer.

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