Combination of PTEN and γ-Ionizing Radiation Enhances Cell Death and G2/M Arrest Through Regulation of AKT Activity and p21 Induction in Non–Small-Cell Lung Cancer Cells

Park, Jong Kuk; Jung, Hae-Yun; Park, Seon Ho; Kang, Seung Yi; Yi, Mi-Rang; Um, Hong Duck; Hong, Sung Hee

doi:10.1016/j.ijrobp.2007.11.069

Cited by 37 publications

(34 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Directly restoring PTEN function has previously been reported to be a valuable approach to radiosensitization (14,31). Our data suggest that silencing miR-221/-222 has synergistic effects on radiation sensitivity.…”

Section: Discussionsupporting

confidence: 55%

MicroRNA-221 and -222 Regulate Radiation Sensitivity by Targeting the PTEN Pathway

Zhang

Kang

Wang

et al. 2011

International Journal of Radiation Oncology*Biology*Physics

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 55%

MicroRNA-221 and -222 Regulate Radiation Sensitivity by Targeting the PTEN Pathway

Zhang

Kang

Wang

et al. 2011

International Journal of Radiation Oncology*Biology*Physics

View full text Add to dashboard Cite

“…However, elimination of CREB protein failed to block migration and invasion perfectly, which imply that other signaling pathways or proteins might also affect migration and invasion in our system. The enhancement of cell migration and invasion by ICAM-3 in NCI-H1299 cells did not show a relationship between ICAM-3, p53 and PTEN because NCI-H1299 cell line is p53-or PTEN-null, but NCI-H460 cell line contains wild-type p53 and PTEN (28). Several previous reports presented that both p53 and PTEN, major tumor suppressors, regulate cell migration and invasion (38-40); Moskovits et al and Gadea et al presented that p53 inhibits cell migration and invasion through suppression of chemokine stromal cellderived factor 1 (SDF-1/CXCL12) expression level and Figure 5.…”

Section: Discussionmentioning

confidence: 87%

“…PcDNA3 and ICAM-3 NCI-H1299 stable transfectants were harvested and nuclei were isolated as previously described (28). Electrophoretic mobility shift assay (EMSA) system was purchased from Promega (Madison, WI, USA) and all procedures were performed as described by the manufacturer.…”

Section: Methodsmentioning

confidence: 99%

ICAM-3 enhances the migratory and invasive potential of human non-small cell lung cancer cells by inducing MMP-2 and MMP-9 via Akt and CREB

Park

et al. 2009

Int J Oncol

View full text Add to dashboard Cite

Abstract.We have previously reported that intercellular adhesion molecule-3 (ICAM-3) is associated with an increase of cellular radio-resistance and cancer cell proliferation. In this study, we hypothesized that ICAM-3 has an additional effect on cancer cell migration and invasion because molecules induced by ICAM-3 are known as regulators of cell migration and invasion. To examine this hypothesis, we used NCI-H1299 non-small cell lung cancer (NSCLC) cell line (p53 and PTEN null cell) and constructed an ICAM-3-over-expressing stable transfectant, which exhibited increased cell migration and invasion. The increased migration and invasion resulted from up-regulation of expression and activities of MMP-2 and MMP-9. ICAM-3 also increased Akt phosphorylation, which caused an increase in cellular migration/invasion and MMP activities. Activity of several transcriptional factors located downstream in the Akt pathway was also tested, and constitutive activation of adenosine 3', 5'-monophosphate response element-binding protein (CREB) by ICAM-3 was detected. Blockage of the Akt pathway attenuated CREB activation, and a decrease in CREB expression reduced cellular migration/invasion and activity of MMPs. This result indicates that CREB functions in the signaling pathway between Akt and MMP. We also showed ICAM-3-induced cell migration and invasion in NCI-H460 NSCLC cells (wild-type p53 and PTEN cell) through the same signaling pathway. Taken together, our findings suggest that ICAM-3 stimulates cancer cell migration/ invasion via ICAM-3/Akt/CREB/MMP pathway regardless of p53 and PTEN status, and this reflects the possibility that ICAM-3 could be considered as a candidate for anti-cancer drug development and as a cancer diagnostic marker.

show abstract

“…Also, PTEN is reportedly involved in the complex response to IR via inducing cell cycle G 2 /M arrest and apoptosis and in sensitizing cells to radiochemotherapy. 15,16 Accordingly, we hypothesized that PTEN is responsible for radioresistance mediated by miR-205. To address this hypothesis, we analyzed PTEN protein and mRNA level in the miR-205-overexpressing CNE-2 cell (CNE-2/miR-205), using CNE-2/vector as a control.…”

Section: Discussionmentioning

confidence: 99%

MiR-205 determines the radioresistance of human nasopharyngeal carcinoma by directly targeting PTEN

et al. 2012

View full text Add to dashboard Cite

Combination of PTEN and γ-Ionizing Radiation Enhances Cell Death and G2/M Arrest Through Regulation of AKT Activity and p21 Induction in Non–Small-Cell Lung Cancer Cells

Cited by 37 publications

References 33 publications

MicroRNA-221 and -222 Regulate Radiation Sensitivity by Targeting the PTEN Pathway

MicroRNA-221 and -222 Regulate Radiation Sensitivity by Targeting the PTEN Pathway

ICAM-3 enhances the migratory and invasive potential of human non-small cell lung cancer cells by inducing MMP-2 and MMP-9 via Akt and CREB

MiR-205 determines the radioresistance of human nasopharyngeal carcinoma by directly targeting PTEN

Contact Info

Product

Resources

About