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Updated: Dec 30, 2025

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Published on: October 27, 2014
The RNA-binding protein Sam68 is critical for non-small cell lung cancer cell proliferation by regulating
Xuebing Li1, Xuexia Zhou2, Feng Hua3
1Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital Tianjin, P. R. China.
Abstract:
Src associated in mitosis, 68 kDa (Sam68) is a KH domain RNA-binding protein that regulates a broad scope of biological events, including RNA metabolism, transcription and signal transduction. Herein, we aimed to explore the expression, clinical significance and biological function of Sam68 in human non-small cell lung cancer (NSCLC). By applying quantitative real-time PCR (qRT-PCR), western blotting and immunohistochemistry (IHC) methods, we found that nucleic localized Sam68 was markedly overexpressed in NSCLC tissues and cell lines. By X2 analysis and Kaplan-Meier survivial analysis between Sam68 expression and various clinicopathological features, Sam68 was found to be significantly associated with clinical T stage, advanced tumor grade, and short overall survival. Finally, in vitro loss-of-function studies showed that knockdown of Sam68 inhibited cell proliferation, colony formation and cell cycle progression in NSCLC cells. Moreover, our results clarified that knockdown of Sam68 could suppress NSCLC cell proliferation via the inhibition of Wnt/β-catenin pathway. To conclude, our results demonstrated that upregulation of Sam68 in NSCLC resulted in poor prognosis, and it promoted cell proliferation via activating Wnt/β-catenin signaling pathway, which could serve as a novel biomarker for the prognosis and therapy of NSCLC.
Insights
Src associated in mitosis, 68 kDa (Sam68) is overexpressed in non-small cell lung cancer (NSCLC), correlating with poor prognosis. Inhibiting Sam68 suppresses NSCLC cell growth by blocking the Wnt/β-catenin pathway, suggesting Sam68 as a therapeutic target.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- Sam68 is an RNA-binding protein regulating diverse cellular processes.
- Its role in non-small cell lung cancer (NSCLC) remains largely unexplored.
Purpose of the Study:
- To investigate the expression, clinical significance, and biological function of Sam68 in NSCLC.
- To determine if Sam68 could serve as a prognostic biomarker and therapeutic target for NSCLC.
Main Methods:
- Quantitative real-time PCR (qRT-PCR), Western blotting, and immunohistochemistry (IHC) were used to assess Sam68 expression.
- Statistical analyses (X², Kaplan-Meier) correlated Sam68 levels with clinicopathological features and survival.
- In vitro loss-of-function studies (siRNA-mediated knockdown) evaluated Sam68's impact on NSCLC cell behavior and signaling pathways.
Main Results:
- Sam68 was significantly overexpressed in NSCLC tissues and cell lines.
- High Sam68 expression correlated with advanced clinical T stage, higher tumor grade, and shorter overall survival.
- Sam68 knockdown inhibited NSCLC cell proliferation, colony formation, and cell cycle progression, primarily through the Wnt/β-catenin pathway.
Conclusions:
- Upregulation of Sam68 in NSCLC is associated with poor prognosis.
- Sam68 promotes NSCLC cell proliferation by activating the Wnt/β-catenin signaling pathway.
- Sam68 represents a potential novel biomarker for NSCLC prognosis and a therapeutic target.
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