Hedgehog Gli3 activator signal augments tumorigenicity of colorectal cancer via upregulation of adherence-related genes

Hironori Iwasaki; Kenji Nakano; Kentaro Shinkai; Yumi Kunisawa; Minako Hirahashi; Yoshinao Oda; Hideya Onishi; Mitsuo Katano

doi:10.1111/cas.12073

Hedgehog Gli3 activator signal augments tumorigenicity of colorectal cancer via upregulation of adherence-related genes

Hironori Iwasaki, Kenji Nakano, Kentaro Shinkai, Yumi Kunisawa, Minako Hirahashi, Yoshinao Oda, Hideya Onishi, Mitsuo Katano

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22 Citations (Scopus)

Abstract

Hedgehog signal is re-activated in several cancers. In this study, we examined the role of Gli3 on malignant phenotype of tumorigenicity for colorectal cancer and its relationship with p53, WNT and ERK/AKT signals. Gli3 expression was detected in HT29 and SW480 (p53-mutant) cells, but not in DLD-1 (p53-mutant) or HCT116 (p53-wild type) cells by reverse transcription-polymerase chain reaction and immunocytochemistry. Full-length Gli3 transfection increased anchor-independent growth for all cells regardless of p53 status, with upregulation of adhesion-related genes. Exogenous Sonic-Hedgehog increased activator-type of Gli3 and colony formation in Gli3-positive HT29 and SW480 cells. After implantation of Gli3-FL or mock-transfectant DLD-1 cells into SCID mice, tumor formation was highly observed in only Gli3-FL-transfectant group. In clinical specimens, Gli3 expression was detected in subsets of colorectal cancer and related with poorly-differentiated histological type, while Sonic-Hedgehog was present with high incidence. In conclusion, activator Gli3 signal augments tumorigenicity of colorectal cancer irrespective of p53 status.

Original language	English
Pages (from-to)	328-336
Number of pages	9
Journal	Cancer Science
Volume	104
Issue number	3
DOIs	https://doi.org/10.1111/cas.12073
Publication status	Published - Mar 1 2013

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All Science Journal Classification (ASJC) codes

Oncology
Cancer Research

Cite this

Iwasaki, H., Nakano, K., Shinkai, K., Kunisawa, Y., Hirahashi, M., Oda, Y., ... Katano, M. (2013). Hedgehog Gli3 activator signal augments tumorigenicity of colorectal cancer via upregulation of adherence-related genes. Cancer Science, 104(3), 328-336. https://doi.org/10.1111/cas.12073

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abstract = "Hedgehog signal is re-activated in several cancers. In this study, we examined the role of Gli3 on malignant phenotype of tumorigenicity for colorectal cancer and its relationship with p53, WNT and ERK/AKT signals. Gli3 expression was detected in HT29 and SW480 (p53-mutant) cells, but not in DLD-1 (p53-mutant) or HCT116 (p53-wild type) cells by reverse transcription-polymerase chain reaction and immunocytochemistry. Full-length Gli3 transfection increased anchor-independent growth for all cells regardless of p53 status, with upregulation of adhesion-related genes. Exogenous Sonic-Hedgehog increased activator-type of Gli3 and colony formation in Gli3-positive HT29 and SW480 cells. After implantation of Gli3-FL or mock-transfectant DLD-1 cells into SCID mice, tumor formation was highly observed in only Gli3-FL-transfectant group. In clinical specimens, Gli3 expression was detected in subsets of colorectal cancer and related with poorly-differentiated histological type, while Sonic-Hedgehog was present with high incidence. In conclusion, activator Gli3 signal augments tumorigenicity of colorectal cancer irrespective of p53 status.",

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10.1111/cas.12073