Knockdown of Hop downregulates RhoC expression, and decreases pseudopodia formation and migration in cancer cell lines

2013 ◽  
Vol 328 (2) ◽  
pp. 252-260 ◽  
Author(s):  
Tarryn Willmer ◽  
Lara Contu ◽  
Gregory L. Blatch ◽  
Adrienne L. Edkins
2020 ◽  
Vol 13 ◽  
Author(s):  
Bashir Mosayyebi ◽  
Leila Mohammadi ◽  
Ashkan Kalantary-Charvadeh ◽  
Mohammad Rahmati

Background: Cell adhesion as dynamic interactions between cell-cell and cell-matrix, has an essential role in cancer cell migration. Integrins as cell membrane receptors are involved in cell adhesion and signal transduction. Aberrant expression of integrins is associated with the cancer cell adhesion. Objective: Targeting the process of cell adhesion and migration could be helpful to prevent cancer cell metastasis. Amygdalin is a cyanoglycoside compound with anti-cancer properties, while its effect on cancer cell adhesion is not completely clear. Methods: The cytotoxic effect of amygdalin on breast cancer cell lines (MCF-7 and MDA-MB-231) and human skin fibroblast cell line as a normal cell, was evaluated through MTT assay. The cell adhesion assay and wound healing assay were performed to determine amygdalin effects on adhesion and migration of cancer cells. Further analysis was carried out to evaluate integrin α and β levels through real-time PCR. Results: We demonstrated that amygdalin diminished the cell viability of both cell lines in a time and dose-dependent manner, while amygdalin did not have any toxicity on human skin fibroblast cell line in same dosages. Following amygdalin treatment, the adhesion of both studied cell lines to fibronectin and collagen I decrease, and this reduction is significantly greater in the case of binding to fibronectin compared to binding to collagen. The MDA-MB-231 cell migration was decreased greater than MCF-7 cells. The levels of α and β integrin were differentially regulated by amygdalin in both cancer cell lines. Conclusion: These results suggest that depending on cancer cell lines, amygdalin affects cancer cell adhesion and migration.


Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 478 ◽  
Author(s):  
Tiziana Tataranni ◽  
Francesca Agriesti ◽  
Consiglia Pacelli ◽  
Vitalba Ruggieri ◽  
Ilaria Laurenzana ◽  
...  

Targeting metabolism represents a possible successful approach to treat cancer. Dichloroacetate (DCA) is a drug known to divert metabolism from anaerobic glycolysis to mitochondrial oxidative phosphorylation by stimulation of PDH. In this study, we investigated the response of two pancreatic cancer cell lines to DCA, in two-dimensional and three-dimension cell cultures, as well as in a mouse model. PANC-1 and BXPC-3 treated with DCA showed a marked decrease in cell proliferation and migration which did not correlate with enhanced apoptosis indicating a cytostatic rather than a cytotoxic effect. Despite PDH activation, DCA treatment resulted in reduced mitochondrial oxygen consumption without affecting glycolysis. Moreover, DCA caused enhancement of ROS production, mtDNA, and of the mitophagy-marker LC3B-II in both cell lines but reduced mitochondrial fusion markers only in BXPC-3. Notably, DCA downregulated the expression of the cancer stem cells markers CD24/CD44/EPCAM only in PANC-1 but inhibited spheroid formation/viability in both cell lines. In a xenograft pancreatic cancer mouse-model DCA treatment resulted in retarding cancer progression. Collectively, our results clearly indicate that the efficacy of DCA in inhibiting cancer growth mechanistically depends on the cell phenotype and on multiple off-target pathways. In this context, the novelty that DCA might affect the cancer stem cell compartment is therapeutically relevant.


2019 ◽  
Vol 38 (10) ◽  
pp. 1132-1144 ◽  
Author(s):  
Y He ◽  
X Cao ◽  
Y Kong ◽  
S Wang ◽  
Y Xia ◽  
...  

Background: Gastric cancer is a malignant tumor with high incidence rate and mortality rate. Purpose: In this study, we investigated the anti-cancer effect of alantolactone, a sesquiterpene lactone, on gastric cancer cell lines BGC-823 and SGC-7901. Methods: BGC-823 and SGC-7901 cells were treated with different concentrations of alantolactone, Hoechst 33258 staining, flow cytometry, wound healing assay, invasion assay, colony forming assay, quantative polymerase chain reaction, and western blot analysis were used to evaluate the anticancer activity of alantolactone to gastric cancer. Results: Alantolactone induced apoptosis of gastric cancer cells by regulating the expression of Bax, Bcl-2, and p53, which related to intrinsic apoptotic pathway, and suppressed colony formation, migration, and invasion by mediating the expression of matrix metalloproteinase (MMP)-2, MMP-7, and MMP-9. Cell signaling pathway analysis showed that alantolactone enhanced the phosphorylation of p38 and decreased the translocation of nucleus p65, suggesting that the apoptosis-promoting and migration-suppressing effect of alantolactone might at least partially rely on regulating p38 mitogen-activated protein kinase (p38MAPK) pathway and nuclear factor-κB (NF-κB) pathway. Conclusions: Alantolactone can be used as a potential therapeutic agent for treating gastric cancer.


Pancreatology ◽  
2013 ◽  
Vol 13 (1) ◽  
pp. 72-78 ◽  
Author(s):  
Lei He ◽  
Fan Wang ◽  
Wei-Qi Dai ◽  
Dong Wu ◽  
Chun-Lei Lin ◽  
...  

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