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Updated: Mar 2, 2026

Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis
Published on: January 31, 2025
Oncogenic function of TUSC3 in non-small cell lung cancer is associated with Hedgehog signalling pathway
Ye Gu1, Xiaojuan Pei2, Yansong Ren1
1Department of Pathology, Nanfang Hospital & School of Basic Medicine, Southern Medical University, 1838 Guangzhou Avenue, Guangzhou 510515, PR China; Guangdong Provincial Key Laboratory of Molecular Tumor Pathology, 1838 Guangzhou Avenue, Guangzhou 510515, PR China.
Abstract:
Non-small cell lung cancer (NSCLC) represents 75-80% of all lung carcinomas, which is the most common cause of death from cancer. Tumour suppressor candidate 3 (TUSC3) is pivotal in many biochemical functions and cytological processes. Dis-regulation of TUSC3 is frequently observed in epithelial cancers. In this study, we observed up-regulated TUSC3 expression at the mRNA and protein levels in clinical NSCLC samples compared with adjacent non-tumorous lung tissues. The expression level of TUSC3 is significantly correlated with tumour metastasis and patient survival. Overexpression of TUSC3 in NSCLC cells led to increased proliferation, migration, and invasion in vitro and accelerated xenograft tumour growth in vivo, while the opposite effects were achieved in TUSC3-silenced cells. Increased GLI1, SMO, PTCH1, and PTCH2 abundance were observed in TUSC3 overexpressed cells using western blotting. Co-immunoprecipitation and immunofluorescence analyses further revealed interaction between TUSC3 and GLI1. In conclusion, our study demonstrated an oncogenic role of TUSC3 in NSCLC and showed that dis-regulation of TUSC3 may affect tumour cell invasion and migration through possible involvement in the Hedgehog (Hh) signalling pathway.
Insights
Tumour suppressor candidate 3 (TUSC3) is upregulated in non-small cell lung cancer (NSCLC), promoting tumour growth and metastasis. TUSC3 may drive NSCLC progression via the Hedgehog signalling pathway.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Non-small cell lung cancer (NSCLC) is a leading cause of cancer mortality.
- Tumour suppressor candidate 3 (TUSC3) plays a role in cellular functions and is dysregulated in epithelial cancers.
Purpose of the Study:
- To investigate the role of TUSC3 in NSCLC.
- To explore the mechanism by which TUSC3 affects NSCLC progression.
Main Methods:
- Analysis of TUSC3 expression in NSCLC tissues and cells.
- In vitro and in vivo experiments to assess the functional impact of TUSC3.
- Western blotting, co-immunoprecipitation, and immunofluorescence to study protein interactions and pathway involvement.
Main Results:
- TUSC3 expression is upregulated in NSCLC and correlates with metastasis and survival.
- TUSC3 overexpression enhances NSCLC cell proliferation, migration, invasion, and tumour growth.
- TUSC3 interacts with GLI1, suggesting involvement in the Hedgehog signalling pathway.
Conclusions:
- TUSC3 acts as an oncogene in NSCLC.
- TUSC3 dysregulation contributes to NSCLC cell invasion and migration, potentially through the Hedgehog pathway.
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