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CDO, an Hh-coreceptor, mediates lung cancer cell proliferation and tumorigenicity through Hedgehog signaling.

Leem YE, Ha HL, Bae JH, Baek KH, Kang JS - PLoS ONE (2014)

Bottom Line: In this study we investigated a role of CDO, an Hh co-receptor, in non-small cell lung cancer (NSCLC).Inhibition of Hh signaling by SANT-1 or siCDO in lung cancer cells reduced proliferation and tumorigenicity, along with the decrease in the expression of the Hh components.These data suggest that CDO is required for proliferation and survival of lung cancer cells via Hh signaling.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, 440-746, Republic of Korea.

ABSTRACT
Hedgehog (Hh) signaling plays essential roles in various developmental processes, and its aberrant regulation results in genetic disorders or malignancies in various tissues. Hyperactivation of Hh signaling is associated with lung cancer development, and there have been extensive efforts to investigate how to control Hh signaling pathway and regulate cancer cell proliferation. In this study we investigated a role of CDO, an Hh co-receptor, in non-small cell lung cancer (NSCLC). Inhibition of Hh signaling by SANT-1 or siCDO in lung cancer cells reduced proliferation and tumorigenicity, along with the decrease in the expression of the Hh components. Histological analysis with NSCLC mouse tissue demonstrated that CDO was expressed in advanced grade of the cancer, and precisely co-localized with GLI1. These data suggest that CDO is required for proliferation and survival of lung cancer cells via Hh signaling.

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Knockdown of CDO in NSCLCs showed the reduction of in vitro and in vivo tumorigenesis.A. Colony formation of the control or CDO knockdown A549, H1299, H460 and H520 in soft agar. B. Quantitative analysis of the experiment described in A. Colony numbers per field were determined by ImageJ. The values represent means of triplicate determinations ±1 SD. *p<0.05 and ** p <0.01. C. Representative tumor growth 50 days after subcutaneous injection of nude mice with the control or shCDO-treated A549 cells. D. The tumor volume of the nude mice with the control A549 (n = 8) or CDO-depleted A549 (n = 10) described in C. Means are shown as error bars. E. Tumors from the nude mice injected with the control A549 or CDO-depleted A549 cells shown in C.
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pone-0111701-g003: Knockdown of CDO in NSCLCs showed the reduction of in vitro and in vivo tumorigenesis.A. Colony formation of the control or CDO knockdown A549, H1299, H460 and H520 in soft agar. B. Quantitative analysis of the experiment described in A. Colony numbers per field were determined by ImageJ. The values represent means of triplicate determinations ±1 SD. *p<0.05 and ** p <0.01. C. Representative tumor growth 50 days after subcutaneous injection of nude mice with the control or shCDO-treated A549 cells. D. The tumor volume of the nude mice with the control A549 (n = 8) or CDO-depleted A549 (n = 10) described in C. Means are shown as error bars. E. Tumors from the nude mice injected with the control A549 or CDO-depleted A549 cells shown in C.

Mentions: The diminished cell proliferation in CDO knockdown led us to investigate the influence of CDO depletion on malignant features of NSCLC cells. For that, we assessed the extent of colony formation of siCDO-transfected A549, H1299, H460 and H520 cells in soft agar (Figure 3A and B). The result displayed a marked reduction in clonogenicity in vitro when CDO level was decreased.


CDO, an Hh-coreceptor, mediates lung cancer cell proliferation and tumorigenicity through Hedgehog signaling.

Leem YE, Ha HL, Bae JH, Baek KH, Kang JS - PLoS ONE (2014)

Knockdown of CDO in NSCLCs showed the reduction of in vitro and in vivo tumorigenesis.A. Colony formation of the control or CDO knockdown A549, H1299, H460 and H520 in soft agar. B. Quantitative analysis of the experiment described in A. Colony numbers per field were determined by ImageJ. The values represent means of triplicate determinations ±1 SD. *p<0.05 and ** p <0.01. C. Representative tumor growth 50 days after subcutaneous injection of nude mice with the control or shCDO-treated A549 cells. D. The tumor volume of the nude mice with the control A549 (n = 8) or CDO-depleted A549 (n = 10) described in C. Means are shown as error bars. E. Tumors from the nude mice injected with the control A549 or CDO-depleted A549 cells shown in C.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4219762&req=5

pone-0111701-g003: Knockdown of CDO in NSCLCs showed the reduction of in vitro and in vivo tumorigenesis.A. Colony formation of the control or CDO knockdown A549, H1299, H460 and H520 in soft agar. B. Quantitative analysis of the experiment described in A. Colony numbers per field were determined by ImageJ. The values represent means of triplicate determinations ±1 SD. *p<0.05 and ** p <0.01. C. Representative tumor growth 50 days after subcutaneous injection of nude mice with the control or shCDO-treated A549 cells. D. The tumor volume of the nude mice with the control A549 (n = 8) or CDO-depleted A549 (n = 10) described in C. Means are shown as error bars. E. Tumors from the nude mice injected with the control A549 or CDO-depleted A549 cells shown in C.
Mentions: The diminished cell proliferation in CDO knockdown led us to investigate the influence of CDO depletion on malignant features of NSCLC cells. For that, we assessed the extent of colony formation of siCDO-transfected A549, H1299, H460 and H520 cells in soft agar (Figure 3A and B). The result displayed a marked reduction in clonogenicity in vitro when CDO level was decreased.

Bottom Line: In this study we investigated a role of CDO, an Hh co-receptor, in non-small cell lung cancer (NSCLC).Inhibition of Hh signaling by SANT-1 or siCDO in lung cancer cells reduced proliferation and tumorigenicity, along with the decrease in the expression of the Hh components.These data suggest that CDO is required for proliferation and survival of lung cancer cells via Hh signaling.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, 440-746, Republic of Korea.

ABSTRACT
Hedgehog (Hh) signaling plays essential roles in various developmental processes, and its aberrant regulation results in genetic disorders or malignancies in various tissues. Hyperactivation of Hh signaling is associated with lung cancer development, and there have been extensive efforts to investigate how to control Hh signaling pathway and regulate cancer cell proliferation. In this study we investigated a role of CDO, an Hh co-receptor, in non-small cell lung cancer (NSCLC). Inhibition of Hh signaling by SANT-1 or siCDO in lung cancer cells reduced proliferation and tumorigenicity, along with the decrease in the expression of the Hh components. Histological analysis with NSCLC mouse tissue demonstrated that CDO was expressed in advanced grade of the cancer, and precisely co-localized with GLI1. These data suggest that CDO is required for proliferation and survival of lung cancer cells via Hh signaling.

Show MeSH
Related in: MedlinePlus