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The Soft Agar Colony Formation Assay
Published on: October 27, 2014
Krüppel-like factor 9 was down-regulated in esophageal squamous cell carcinoma and negatively regulated
Fan Qiao1, Feng Yao2, Ling Chen1
1Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China.
Abstract:
Krüppel-like factor 9 (KLF9) has been found to play suppressive roles in several types of tumor. However, the expression pattern and biological functions of KLF9 in esophageal squamous cell carcinoma (ESCC) are still unknown. In this study, it was found that the expression of KLF9 was significantly down-regulated in ESCC compared to their adjacent normal esophageal tissues. Meanwhile, the expression of KLF9 was inversely correlated with the clinical features of ESCC patients. Moreover, in the biological function study, KLF9 was further validated to inhibit the growth, migration, and metastasis of ESCC cells in vitro and in vivo. Mechanistically, KLF9 bind with TCF4 and suppressed the beta-catenin/TCF signaling as well as the expression of its target gene Cyr61. Collectively, our study clarified the function of KLF9 in both ESCC progression and the regulation of beta-catenin/TCF signaling.
Insights
Krüppel-like factor 9 (KLF9) is down-regulated in esophageal squamous cell carcinoma (ESCC), inhibiting tumor growth and metastasis. KLF9 suppresses beta-catenin/TCF signaling, offering a potential therapeutic target for ESCC.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Krüppel-like factor 9 (KLF9) exhibits tumor-suppressive roles in various cancers.
- The role of KLF9 in esophageal squamous cell carcinoma (ESCC) remains largely uncharacterized.
Purpose of the Study:
- To investigate the expression pattern and biological functions of KLF9 in ESCC.
- To elucidate the underlying molecular mechanisms of KLF9's action in ESCC progression.
Main Methods:
- Quantitative analysis of KLF9 expression in ESCC tissues versus normal tissues.
- In vitro and in vivo assays to assess the effects of KLF9 on ESCC cell growth, migration, and metastasis.
- Mechanistic studies involving KLF9 binding to TCF4 and its impact on the beta-catenin/TCF signaling pathway and Cyr61 expression.
Main Results:
- KLF9 expression is significantly downregulated in ESCC tissues compared to adjacent normal tissues.
- Downregulation of KLF9 correlates inversely with clinical features in ESCC patients.
- KLF9 inhibits ESCC cell proliferation, migration, and metastasis both in vitro and in vivo.
- KLF9 suppresses the beta-catenin/TCF signaling pathway by interacting with TCF4 and downregulating Cyr61.
Conclusions:
- KLF9 acts as a tumor suppressor in ESCC.
- KLF9 negatively regulates ESCC progression by inhibiting the beta-catenin/TCF signaling pathway.
- KLF9 represents a potential therapeutic target for managing ESCC.
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