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Updated: Sep 20, 2026

In vitro Organoid Culture of Primary Mouse Colon Tumors
Published on: May 17, 2013
[Stat3 signal transduction pathway orchestrates G1 to S cell cycle transition in colon cancer cells]
Xiangtao Ma1, Shan Wang, Ruyu Du
1Department II of Surgery, Laboratory of Surgical Oncology, Peking University People's Hospital, Beijing 100044, China. tonyma72@yahoo.com.cn
Objective:
To show that Stat3 plays a key role in the G1 to S phase transition in colon cancer cells.
Methods:
Human colon cancer cell lines SW480 and HCT116 were transfected with Stat3 antisense oligonucleotide mediated by liposome, MTT assay was used to measure the proliferation, flow cytometry was applied to analyze the cell cycle, and the expressions of Stat3, phosphorylation-specific Stat3 (tyrosine 705), Cyclin D1, Cyclin E, CDK2, CDK4, CDK6, p21 and p27 were measured by western blot.
Results:
SW480 and HCT116 colon cancer cell lines expressed constitutively activated Stat3. Targeting of Stat3 using antisense oligonucleotide which directed against the translation site resulted in growth inhibition, downregulation of Stat3, p-Stat3, Cyclins and CDKs, and up-regulation of p21 and p27.
Conclusion:
Our findings suggest that Stat3 plays an important role in the G1 to S phase transition in colon cancer cells, Stat3 orchestrates cell cycle by regulating the balance between CDK/Cyclin complex and CKI.
Insights
Signal transducer and activator of transcription 3 (Stat3) is crucial for colon cancer cell cycle progression. Inhibiting Stat3 halts cell proliferation by regulating G1 to S phase transition.
Area of Science:
- Molecular biology
- Cancer research
- Cell cycle regulation
Context:
- Constitutively activated Signal transducer and activator of transcription 3 (Stat3) is observed in human colon cancer cell lines SW480 and HCT116.
- Stat3 signaling is implicated in various cancers, but its precise role in colon cancer cell cycle progression requires further elucidation.
Purpose:
- To investigate the role of Stat3 in the G1 to S phase transition of colon cancer cells.
- To determine the effect of Stat3 inhibition on colon cancer cell proliferation and cell cycle regulators.
Summary:
- Human colon cancer cell lines SW480 and HCT116 were treated with Stat3 antisense oligonucleotide.
- Cell proliferation was assessed using MTT assay, and cell cycle distribution was analyzed by flow cytometry.
- Western blot analysis measured the expression of Stat3, phosphorylated Stat3 (p-Stat3), Cyclins (D1, E), Cyclin-dependent kinases (CDKs: 2, 4, 6), and CDK inhibitors (p21, p27).
Impact:
- Targeting Stat3 with antisense oligonucleotides inhibited colon cancer cell growth.
- Stat3 inhibition led to downregulation of Stat3, p-Stat3, Cyclins, and CDKs, and upregulation of p21 and p27.
- These findings indicate Stat3's critical role in orchestrating the G1 to S phase transition by modulating the balance between CDK/Cyclin complexes and CDK inhibitors in colon cancer.
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