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Updated: Mar 25, 2026
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Isolation of CD133+ Liver Stem Cells for Clonal Expansion
Published on: October 10, 2011
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CD133 promotes gallbladder carcinoma cell migration through activating Akt phosphorylation.
Chen Li1, Cong Wang1, Yang Xing2
1Zhongshan Hospital of Fudan University, Shanghai, People's Republic of China.
Oncotarget
|February 25, 2016
Summary
CD133, a cancer stem cell marker, is highly expressed in gallbladder carcinoma (GBC) and promotes metastasis. Reducing CD133 inhibits GBC cell migration by affecting the Akt signaling pathway.
Area of Science:
- Oncology
- Gastroenterology
- Cancer Biology
Background:
- Gallbladder carcinoma (GBC) has a poor prognosis, often due to metastasis.
- Mechanisms driving GBC metastasis are not well understood.
- CD133 is a known cancer stem cell marker implicated in various cancers, including GBC.
Purpose of the Study:
- To investigate the role of CD133 in gallbladder carcinoma metastasis.
- To elucidate the molecular mechanisms by which CD133 influences GBC cell migration and invasion.
Main Methods:
- Comparative analysis of CD133 expression in GBC and normal tissues.
- Assessment of CD133's effect on GBC cell migration, invasion, and proliferation.
- Investigation of the Akt signaling pathway, including Akt phosphorylation and PTEN levels.
- Functional rescue experiments using Akt activators and inhibitors.
Main Results:
- CD133 is highly expressed in GBC, particularly in invasive areas.
- Down-regulation of CD133 significantly inhibited GBC cell migration and invasion without affecting proliferation.
- CD133 down-regulation led to decreased Akt phosphorylation and increased PTEN protein levels.
- Akt pathway modulation rescued or inhibited GBC cell migration.
Conclusions:
- CD133 plays a crucial role in promoting gallbladder carcinoma cell migration and invasion.
- The inhibitory effect of CD133 down-regulation on metastasis is mediated through the Akt signaling pathway.
- Targeting CD133 may offer a therapeutic strategy for inhibiting GBC progression.
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