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DDX5 promotes proliferation and tumorigenesis of non-small-cell lung cancer cells by activating β-catenin signaling pathway.

Wang Z, Luo Z, Zhou L, Li X, Jiang T, Fu E - Cancer Sci. (2015)

Bottom Line: The DEAD-box-protein DDX5 is an ATP-dependent RNA helicase that is frequently overexpressed in various cancers and acts as a transcriptional co-activator of several transcription factors, including β-catenin.DDX5 is reported to be involved in cancer progression by promoting cell proliferation and epithelial-mesenchymal transition.We found that DDX5 was significantly overexpressed in NSCLC tissues as compared with the matched normal adjacent tissues.

View Article: PubMed Central - PubMed

Affiliation: Department of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, China.

No MeSH data available.


Related in: MedlinePlus

DDX5 promotes non-small-cell lung cancer cell growth in vivo. (a, b) H520 cells were stably infected with the indicated lentivirus and injected s.c. into BALB/c-nude mice. Four weeks after injection, xenografts were removed. Tumor volume and tumor weight were determined. (c) Representative images of xenografts from different groups. (d–f) Immunohistochemical analysis of the expression of DDX5, Ki67, and cyclin D1 in different groups of xenografts. *P < 0.05.
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fig05: DDX5 promotes non-small-cell lung cancer cell growth in vivo. (a, b) H520 cells were stably infected with the indicated lentivirus and injected s.c. into BALB/c-nude mice. Four weeks after injection, xenografts were removed. Tumor volume and tumor weight were determined. (c) Representative images of xenografts from different groups. (d–f) Immunohistochemical analysis of the expression of DDX5, Ki67, and cyclin D1 in different groups of xenografts. *P < 0.05.

Mentions: To confirm the pro-proliferative role of DDX5 in vivo, we established a xenograft model using H520 cells stably infected with DDX5 or DDX5-RNAi, as well as the vectors. As shown in Figure5, DDX5 overexpression resulted in significantly larger tumor size and tumor mass compared with the vector control group; DDX5 downregulation significantly decreased the tumor size and tumor mass relative to the shRNA vector control group. Moreover, IHC staining revealed that tumors formed by cells infected with DDX5 showed a significant increase expression of cyclin D1 and Ki67. In contrast, tumors formed by cells infected with DDX5-RNAi displayed a sharply decreased expression of cyclin D1 and Ki67. Collectively, these data further confirmed that DDX5 had a key role in promoting the proliferation and tumorigenesis of NSCLC cells.


DDX5 promotes proliferation and tumorigenesis of non-small-cell lung cancer cells by activating β-catenin signaling pathway.

Wang Z, Luo Z, Zhou L, Li X, Jiang T, Fu E - Cancer Sci. (2015)

DDX5 promotes non-small-cell lung cancer cell growth in vivo. (a, b) H520 cells were stably infected with the indicated lentivirus and injected s.c. into BALB/c-nude mice. Four weeks after injection, xenografts were removed. Tumor volume and tumor weight were determined. (c) Representative images of xenografts from different groups. (d–f) Immunohistochemical analysis of the expression of DDX5, Ki67, and cyclin D1 in different groups of xenografts. *P < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4638002&req=5

fig05: DDX5 promotes non-small-cell lung cancer cell growth in vivo. (a, b) H520 cells were stably infected with the indicated lentivirus and injected s.c. into BALB/c-nude mice. Four weeks after injection, xenografts were removed. Tumor volume and tumor weight were determined. (c) Representative images of xenografts from different groups. (d–f) Immunohistochemical analysis of the expression of DDX5, Ki67, and cyclin D1 in different groups of xenografts. *P < 0.05.
Mentions: To confirm the pro-proliferative role of DDX5 in vivo, we established a xenograft model using H520 cells stably infected with DDX5 or DDX5-RNAi, as well as the vectors. As shown in Figure5, DDX5 overexpression resulted in significantly larger tumor size and tumor mass compared with the vector control group; DDX5 downregulation significantly decreased the tumor size and tumor mass relative to the shRNA vector control group. Moreover, IHC staining revealed that tumors formed by cells infected with DDX5 showed a significant increase expression of cyclin D1 and Ki67. In contrast, tumors formed by cells infected with DDX5-RNAi displayed a sharply decreased expression of cyclin D1 and Ki67. Collectively, these data further confirmed that DDX5 had a key role in promoting the proliferation and tumorigenesis of NSCLC cells.

Bottom Line: The DEAD-box-protein DDX5 is an ATP-dependent RNA helicase that is frequently overexpressed in various cancers and acts as a transcriptional co-activator of several transcription factors, including β-catenin.DDX5 is reported to be involved in cancer progression by promoting cell proliferation and epithelial-mesenchymal transition.We found that DDX5 was significantly overexpressed in NSCLC tissues as compared with the matched normal adjacent tissues.

View Article: PubMed Central - PubMed

Affiliation: Department of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, China.

No MeSH data available.


Related in: MedlinePlus