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Hedgehog signaling pathway is a potential therapeutic target for gallbladder cancer.

Matsushita S, Onishi H, Nakano K, Nagamatsu I, Imaizumi A, Hattori M, Oda Y, Tanaka M, Katano M - Cancer Sci. (2014)

Bottom Line: New effective therapeutic strategies are greatly needed.In contrast, inhibiting the effector Smo decreased the anchor-dependent and anchor-independent proliferation.These results suggest that Hh signaling is elevated in GBC and may be involved in the acquisition of malignant phenotypes, and that Hh signaling may be a potential therapeutic target for GBC.

View Article: PubMed Central - PubMed

Affiliation: Department of Cancer Therapy and Research, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

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Related in: MedlinePlus

Recombinant human Sonic Hedgehog (rhShh) augments the proliferative and invasive phenotypes of gallbladder cancer cells. (a) GBd15 and TGBC2TKB cells were seeded onto 96-well plates at a density of 5000 cells/well and incubated with rhShh (at 0.1, 1.0, or 2.0 μg/mL) for 24, 48, or 72 h as indicated. (b) GBd15 and TGBC2TKB cells were incubated for 16 h in the presence or absence of rhShh (at 0.1 or 1.0 μg/mL). Migrated cells were quantified by bright-field microscopy. Error bars represent standard deviations. *P < 0.05.
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fig03: Recombinant human Sonic Hedgehog (rhShh) augments the proliferative and invasive phenotypes of gallbladder cancer cells. (a) GBd15 and TGBC2TKB cells were seeded onto 96-well plates at a density of 5000 cells/well and incubated with rhShh (at 0.1, 1.0, or 2.0 μg/mL) for 24, 48, or 72 h as indicated. (b) GBd15 and TGBC2TKB cells were incubated for 16 h in the presence or absence of rhShh (at 0.1 or 1.0 μg/mL). Migrated cells were quantified by bright-field microscopy. Error bars represent standard deviations. *P < 0.05.

Mentions: We hypothesized that Hh signaling may contribute to the malignancy of GBC. We examined the impact of Hh activation on proliferation and invasiveness. The addition of rhShh augmented the proliferation rate (Fig.3a) and invasiveness (Fig.3b) of GBd15 and TGBC2TKB cells. These results indicate that activation of Hh signaling further enhances the proliferative and invasive phenotypes of GBC cells.


Hedgehog signaling pathway is a potential therapeutic target for gallbladder cancer.

Matsushita S, Onishi H, Nakano K, Nagamatsu I, Imaizumi A, Hattori M, Oda Y, Tanaka M, Katano M - Cancer Sci. (2014)

Recombinant human Sonic Hedgehog (rhShh) augments the proliferative and invasive phenotypes of gallbladder cancer cells. (a) GBd15 and TGBC2TKB cells were seeded onto 96-well plates at a density of 5000 cells/well and incubated with rhShh (at 0.1, 1.0, or 2.0 μg/mL) for 24, 48, or 72 h as indicated. (b) GBd15 and TGBC2TKB cells were incubated for 16 h in the presence or absence of rhShh (at 0.1 or 1.0 μg/mL). Migrated cells were quantified by bright-field microscopy. Error bars represent standard deviations. *P < 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317941&req=5

fig03: Recombinant human Sonic Hedgehog (rhShh) augments the proliferative and invasive phenotypes of gallbladder cancer cells. (a) GBd15 and TGBC2TKB cells were seeded onto 96-well plates at a density of 5000 cells/well and incubated with rhShh (at 0.1, 1.0, or 2.0 μg/mL) for 24, 48, or 72 h as indicated. (b) GBd15 and TGBC2TKB cells were incubated for 16 h in the presence or absence of rhShh (at 0.1 or 1.0 μg/mL). Migrated cells were quantified by bright-field microscopy. Error bars represent standard deviations. *P < 0.05.
Mentions: We hypothesized that Hh signaling may contribute to the malignancy of GBC. We examined the impact of Hh activation on proliferation and invasiveness. The addition of rhShh augmented the proliferation rate (Fig.3a) and invasiveness (Fig.3b) of GBd15 and TGBC2TKB cells. These results indicate that activation of Hh signaling further enhances the proliferative and invasive phenotypes of GBC cells.

Bottom Line: New effective therapeutic strategies are greatly needed.In contrast, inhibiting the effector Smo decreased the anchor-dependent and anchor-independent proliferation.These results suggest that Hh signaling is elevated in GBC and may be involved in the acquisition of malignant phenotypes, and that Hh signaling may be a potential therapeutic target for GBC.

View Article: PubMed Central - PubMed

Affiliation: Department of Cancer Therapy and Research, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

Show MeSH
Related in: MedlinePlus