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Cisplatin sensitivity is enhanced in non-small cell lung cancer cells by regulating epithelial-mesenchymal transition through inhibition of eukaryotic translation initiation factor 5A2.

Xu G, Yu H, Shi X, Sun L, Zhou Q, Zheng D, Shi H, Li N, Zhang X, Shao G - BMC Pulm Med (2014)

Bottom Line: Recent studies have suggested eIF5A-2 may function as a proliferation-related oncogene in tumorigenic processes.We found low concentrations of GC7 have little effect on NSCLC viability, but could enhance cisplatin cytotoxicity in NSCLC cells.GC7 also could reverse mesenchymal phenotype in NCI-H1299 and prevented A549 cells undergoing EMT after TGF-β1 inducement. eIF5A-2 knockdown resulted in EMT inhibition.

View Article: PubMed Central - PubMed

Affiliation: Department of Thoracic & Cardiovascular Surgery, Lihuili Hospital, Ningbo Medical Center, Affiliated Hospital of Medical School of Ningbo University, NO 57 Xingning Road, Ningbo 315041, China. guofengshaolihuili@163.com.

ABSTRACT

Background: Epithelial-mesenchymal transition (EMT) has been believed to be related with chemotherapy resistance in non-small cell lung cancer (NSCLC). Recent studies have suggested eIF5A-2 may function as a proliferation-related oncogene in tumorigenic processes.

Methods: We used cell viability assays, western blotting, immunofluorescence, transwell-matrigel invasion assay, wound-healing assay combined with GC7 (a novel eIF5A-2 inhibitor) treatment or siRNA interference to investigate the role of eIF5A-2 playing in NSCLC chemotherapy.

Results: We found low concentrations of GC7 have little effect on NSCLC viability, but could enhance cisplatin cytotoxicity in NSCLC cells. GC7 also could reverse mesenchymal phenotype in NCI-H1299 and prevented A549 cells undergoing EMT after TGF-β1 inducement. eIF5A-2 knockdown resulted in EMT inhibition.

Conclusion: Our data indicated GC7 enhances cisplatin cytotoxicity and prevents the EMT in NSCLC cells by inhibiting eIF5A-2.

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Related in: MedlinePlus

GC7 reverses EMT in NCI-H1299 cells via eIF5A-2 regulation. (A) Western blotting (B) immunofluorescence (C) wound-healing assay (D) Transwell-Matrigel invasion assay.
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Fig6: GC7 reverses EMT in NCI-H1299 cells via eIF5A-2 regulation. (A) Western blotting (B) immunofluorescence (C) wound-healing assay (D) Transwell-Matrigel invasion assay.

Mentions: In order to verify whether eIF5A-2 was a key factor in GC7 regulation of EMT, we transfected eIF5A-2 siRNA into NCI-H1299 cells without carrying out GC7 treatment. The results showed that the transfected NCI-H1299 cells transformed from mesenchymal phenotype to epithelial phenotype (Figure 6A–D). Conversely, when the transfected cells were treated with GC7, the cells stayed as epithelial phenotype (Figure 6A–D).Figure 4


Cisplatin sensitivity is enhanced in non-small cell lung cancer cells by regulating epithelial-mesenchymal transition through inhibition of eukaryotic translation initiation factor 5A2.

Xu G, Yu H, Shi X, Sun L, Zhou Q, Zheng D, Shi H, Li N, Zhang X, Shao G - BMC Pulm Med (2014)

GC7 reverses EMT in NCI-H1299 cells via eIF5A-2 regulation. (A) Western blotting (B) immunofluorescence (C) wound-healing assay (D) Transwell-Matrigel invasion assay.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4232729&req=5

Fig6: GC7 reverses EMT in NCI-H1299 cells via eIF5A-2 regulation. (A) Western blotting (B) immunofluorescence (C) wound-healing assay (D) Transwell-Matrigel invasion assay.
Mentions: In order to verify whether eIF5A-2 was a key factor in GC7 regulation of EMT, we transfected eIF5A-2 siRNA into NCI-H1299 cells without carrying out GC7 treatment. The results showed that the transfected NCI-H1299 cells transformed from mesenchymal phenotype to epithelial phenotype (Figure 6A–D). Conversely, when the transfected cells were treated with GC7, the cells stayed as epithelial phenotype (Figure 6A–D).Figure 4

Bottom Line: Recent studies have suggested eIF5A-2 may function as a proliferation-related oncogene in tumorigenic processes.We found low concentrations of GC7 have little effect on NSCLC viability, but could enhance cisplatin cytotoxicity in NSCLC cells.GC7 also could reverse mesenchymal phenotype in NCI-H1299 and prevented A549 cells undergoing EMT after TGF-β1 inducement. eIF5A-2 knockdown resulted in EMT inhibition.

View Article: PubMed Central - PubMed

Affiliation: Department of Thoracic & Cardiovascular Surgery, Lihuili Hospital, Ningbo Medical Center, Affiliated Hospital of Medical School of Ningbo University, NO 57 Xingning Road, Ningbo 315041, China. guofengshaolihuili@163.com.

ABSTRACT

Background: Epithelial-mesenchymal transition (EMT) has been believed to be related with chemotherapy resistance in non-small cell lung cancer (NSCLC). Recent studies have suggested eIF5A-2 may function as a proliferation-related oncogene in tumorigenic processes.

Methods: We used cell viability assays, western blotting, immunofluorescence, transwell-matrigel invasion assay, wound-healing assay combined with GC7 (a novel eIF5A-2 inhibitor) treatment or siRNA interference to investigate the role of eIF5A-2 playing in NSCLC chemotherapy.

Results: We found low concentrations of GC7 have little effect on NSCLC viability, but could enhance cisplatin cytotoxicity in NSCLC cells. GC7 also could reverse mesenchymal phenotype in NCI-H1299 and prevented A549 cells undergoing EMT after TGF-β1 inducement. eIF5A-2 knockdown resulted in EMT inhibition.

Conclusion: Our data indicated GC7 enhances cisplatin cytotoxicity and prevents the EMT in NSCLC cells by inhibiting eIF5A-2.

Show MeSH
Related in: MedlinePlus