Differential involvement of ERK1‐2 and p38MAPK activation on Swiss 3T3 cell proliferation induced by prostaglandin F2α

Dekanty, Andrés; Giulianelli, Sebastián; Coso, Omar A.; Rudland, Phillip S.; Asua, Luis Adan Felipe Jimenez de

doi:10.1016/j.febslet.2006.03.075

Cited by 4 publications

(3 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The mechanism of the activation of intracellular signaling pathway by PGF2α-regulated is not yet clear. It has repoted that PGF2 could activate MEK/extracellular signal-regulated kinase (ERK) signaling pathways to regulate cell proliferation [32, 33] and angiogenic factor expression [34]. Other reports found that PGF2α -activated signaling pathway is mediated through ERKdependent but Akt-independent pathway [35].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of AKR1C3 significantly enhances human prostate cancer cells resistance to radiation

Sun

Gao

et al. 2016

Oncotarget

View full text Add to dashboard Cite

Aldo-keto reductase 1C3(AKR1C3) is an enzyme involved in prostaglandins metabolism. Studies suggest that AKR1C3 has a pivotal role in the radioresistance of esophageal cancer and non-small-cell lung cancer, yet the role of AKR1C3 in prostate cancer cells radiation resistance has not yet been clarified. In our study, we established a stable overexpressing AKR1C3 cell line (AKR1C3-over) derived from the prostate cell line DU145 and its control cell line (Control). We conducted colony formation assay to determine the role of AKR1C3 in radioresistance and we used its chemical inhibitor to detect whether it can restored the sensitivity of the acquired tumor cells. Flow cytometry assay was carried out to detect IR-induced ROS accumulation. Elisa was adopted to dedect the concentration of PGF2α in the suspension of the cells after 6GY radiation. Western blotting was used to dedect the MAPK and PPAR γ. The results demonstrated that overexpression of AKR1C3 in prostate cancer can result in radioresistance and suppression of AKR1C3 via its chemical inhibitor indocin restored the sensitivity of the acquired tumor cells. According to the flow cytometry assay, ROS was decreased by 80% in DU145-over cells. Also overexpression of AKR1C3 could result in the accumulation of prostaglandin F2α (PGF2α), which can not only promote prostate cancer cell 's proliferation but also could enhance prostate cancer cells resistance to radiation and activated the MAPK pathway and inhibited the expression of PPARγ. In conclusion, we found that overexpression of AKR1C3 significantly enhanced human prostate cancer cells resistance to radiation through activation of MAPK pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Overexpression of AKR1C3 significantly enhances human prostate cancer cells resistance to radiation

Sun

Gao

et al. 2016

Oncotarget

View full text Add to dashboard Cite

show abstract

“…One of the key events in the development of cancer is the overexpression of COX-2. In particular, the tumorigenic role of COX-2 and also its products such as PGE 2 and PGF 2  have been well described during colorectal cancer development [9][10][11][12][13][14][15]. The correlation between COX-2 expression and MIB-1 labeling index was also previously shown in breast, renal and gastric cancers [16][17][18].…”

Section: Introductionmentioning

confidence: 91%

Clinicopathological evaluation of cyclooxygenase-2 expression in meningioma: immunohistochemical analysis of 76 cases of low and high-grade meningioma

et al. 2012

View full text Add to dashboard Cite

“…AKT and Erk1/2 signaling pathways are known to play a key role in cell survival and proliferation, respectively. 34,35 Therefore, ILK could play a role in sustaining the proliferation of the activated HSCs, thus preventing their death by apoptosis. 34 To test this hypothesis we transfected CFSC-2G with ILK siRNA and determined the extent of PKB and MAPKs phosphorylation and HSC proliferation.…”

Section: Mmp-9mentioning

confidence: 99%

Involvement of integrin-linked kinase in carbon tetrachloride–induced hepatic fibrosis in rats

et al. 2006

View full text Add to dashboard Cite

Integrin-linked kinase (ILK) is a multidomain focal adhesion protein implicated in signal transduction between integrins and growth factor receptors. Although its expression is upregulated in pulmonary and renal fibrosis, its role in the development of hepatic fibrosis remains to be determined. Therefore, we considered it important to investigate whether ILK is involved in activation of hepatic stellate cells and thus plays a role in the development of hepatic fibrosis. Immunohistochemical analysis of liver sections obtained from rats with CCl 4 -induced cirrhosis revealed increased expression and colocalization of ILK and alpha-smooth muscle actin in hepatic stellate cells in perisinusoidal areas. In addition, hepatic stellate cells isolated from fibrotic livers expressed high levels of ILK and alpha-smooth muscle actin, and their expression was sustained in culture. In contrast, hepatic stellate cells (HSCs) isolated from normal rat liver did not express ILK, but its expression was increased when the cells were activated in culture. Our studies also showed that ILK is involved in the phosphorylation of ERK 1/2, p38 MAPK, JNK, and PKB and that selective inhibition of ILK expression by siRNA results in a significant decrease in their phosphorylation. These changes were accompanied by significant inhibition of cell spreading and migration without affecting cell proliferation. In conclusion, ILK plays a key role in HSC activation and could be a possible target for antifibrogenic therapy. (HEPATOLOGY 2006;44:612-622.)

show abstract

Differential involvement of ERK_1‐2 and p38^MAPK activation on Swiss 3T3 cell proliferation induced by prostaglandin F_2α

Cited by 4 publications

References 23 publications

Overexpression of AKR1C3 significantly enhances human prostate cancer cells resistance to radiation

Overexpression of AKR1C3 significantly enhances human prostate cancer cells resistance to radiation

Clinicopathological evaluation of cyclooxygenase-2 expression in meningioma: immunohistochemical analysis of 76 cases of low and high-grade meningioma

Involvement of integrin-linked kinase in carbon tetrachloride–induced hepatic fibrosis in rats

Contact Info

Product

Resources

About