Nimbolide retards tumor cell migration, invasion, and angiogenesis by downregulating MMP-2/9 expression via inhibiting ERK1/2 and reducing DNA-binding activity of NF-κB in colon cancer cells

2011 ◽  
Vol 51 (6) ◽  
pp. 475-490 ◽  
Author(s):  
Suboj Babykutty ◽  
Priya P.S. ◽  
Nandini R.J. ◽  
M.A. Suresh Kumar ◽  
Mangalam S. Nair ◽  
...  
2012 ◽  
Vol 45 (5) ◽  
pp. 581-591 ◽  
Author(s):  
Priya Suboj ◽  
Suboj Babykutty ◽  
Deepak Roshan Valiyaparambil Gopi ◽  
Rakesh S. Nair ◽  
Priya Srinivas ◽  
...  

2015 ◽  
Vol 459 (2) ◽  
pp. 327-332 ◽  
Author(s):  
Peng Yang ◽  
Zongwei Li ◽  
Yingying Wang ◽  
Lichao Zhang ◽  
Haili Wu ◽  
...  

2018 ◽  
Vol 48 (4) ◽  
pp. 1556-1562 ◽  
Author(s):  
Yongze Liu ◽  
Han Zhou ◽  
Xiaofeng Ma ◽  
Chuanyao Lin ◽  
Ling Lu ◽  
...  

Background/Aims: Nasopharyngeal carcinoma remains a devastating and difficult disease to treat. This study explores the antineoplastic effect of prodigiosin on nasopharyngeal cancer cells. Methods: Human nasopharyngeal carcinoma CNE2 cells and human normal nasopharyngeal epithelial NP69 cells were obtained and treated with prodigiosin or fluorouracil (5-FU). Colony formation assay was performed to screen for the optimal experimental concentrations of prodigiosin and 5-FU, and MTT assay was used to examine cell proliferative ability. Flow cytometry was used to examine cell cycle distribution, the scratch test was employed to examine cell migration, and Transwell migration assay (Boyden chamber) was used to study cell invasion. Results: The optimal concentrations of prodigiosin and 5-FU for treatment were 4 mg/L and 0.35 mg/L, respectively. Both prodigiosin and 5-FU inhibited tumor cell proliferation. The percentage of cells in G0/G1 phase was higher and the percentage of cells in S phase was lower in the prodigiosin and 5-FU groups than in the untreated groups. Both prodigiosin and 5-FU inhibited tumor cell migration and tumor cell invasion. Conclusions: Our results suggest that prodigiosin can inhibit proliferation, migration, and invasion of nasopharyngeal carcinoma cells.


1999 ◽  
Vol 274 (49) ◽  
pp. 34811-34818 ◽  
Author(s):  
Joseph M. Bosilevac ◽  
Randall J. Olsen ◽  
Julia A. Bridge ◽  
Steven H. Hinrichs

Oncogene ◽  
2015 ◽  
Vol 35 (24) ◽  
pp. 3151-3162 ◽  
Author(s):  
Q Zhang ◽  
T Wei ◽  
K Shim ◽  
K Wright ◽  
K Xu ◽  
...  

Abstract Sprouty (SPRY) appears to act as a tumor suppressor in cancer, whereas we demonstrated that SPRY2 functions as a putative oncogene in colorectal cancer (CRC) (Oncogene, 2010, 29: 5241–5253). We investigated the mechanisms by which SPRY regulates epithelial–mesenchymal transition (EMT) in CRC. SPRY1 and SPRY2 mRNA transcripts were significantly upregulated in human CRC. Suppression of SPRY2 repressed AKT2 and EMT-inducing transcription factors and significantly increased E-cadherin expression. Concurrent downregulation of SPRY1 and SPRY2 also increased E-cadherin and suppressed mesenchymal markers in colon cancer cells. An inverse expression pattern between AKT2 and E-cadherin was established in a human CRC tissue microarray. SPRY2 negatively regulated miR-194-5p that interacts with AKT2 3′ untranslated region. Mir-194 mimics increased E-cadherin expression and suppressed cancer cell migration and invasion. By confocal microscopy, we demonstrated redistribution of E-cadherin to plasma membrane in colon cancer cells transfected with miR-194. Spry1 −/− and Spry2 −/− double mutant mouse embryonic fibroblasts exhibited decreased cell migration while acquiring several epithelial markers. In CRC, SPRY drive EMT and may serve as a biomarker of poor prognosis.


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