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Updated: May 13, 2026

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy
Published on: January 31, 2025
Decrease of autophagy activity promotes malignant progression of tongue squamous cell carcinoma
Yawen Wang1, Cheng Wang, Haikuo Tang
1Department of Oral and Maxillofacial Surgery, Guanghua School and Research Institute of Stomatology, Sun Yat-sen University, Guangzhou, China.
Background:
Autophagy is a catabolic process involving the degradation of cells' own unnecessary, injured, or aged proteins and recycling of degraded products to maintain hemostasis. Recently, studies indicated that autophagy plays a crucial role in cancer development. However, the role of autophagy in tongue squamous cell carcinoma (TSCC) has not been well documented. This study aims to assess the expression of autophagy-related protein and investigate its effect on TSCC.
Materials And Methods:
Archival 50 TSCC samples were enrolled. Immunohistochemistry were performed to examine the expression of Beclin1 and LC3. Statistical analyses were carried out to assess the associations among clinicopathologic parameters. In vitro, cells were treated with rapamycin or 3-MA. Then, qPCR, western blot and immunofluorescence were performed to detect the expression of Beclin1 and LC3. Transmission electron microscopy was utilized to identify autophagsomes. For functional analysis, cell proliferation and cell cycle were evaluated with MTT assay and flow cytometer, respectively. At last, cell migration and invasion potentials were assessed by wound healing assay and transwell assay.
Results:
We confirmed that down-regulation of Beclin1 and LC3 is a frequent event in TSCC. Then, we demonstrated that decreased expression of Beclin1 was associated with T stage, clinical stage and differentiation. Furthermore, we showed that activation of autophagy by rapamycin suppressed proliferation, migration and invasion while inhibition of autophagy by 3-MA promoted proliferation, migration and invasion in TSCC cells.
Conclusion:
Taken together, these data suggest that autophagy plays a pivotal role in the progression of TSCC.
Insights
Autophagy, crucial for cell health, is often down-regulated in tongue squamous cell carcinoma (TSCC). Modulating autophagy impacts TSCC progression, suggesting its therapeutic potential.
Area of Science:
- Oncology
- Cell Biology
- Molecular Biology
Background:
- Autophagy is a cellular degradation process vital for maintaining homeostasis.
- Emerging evidence highlights autophagy's role in cancer development.
- The specific function of autophagy in tongue squamous cell carcinoma (TSCC) remains underexplored.
Purpose of the Study:
- To investigate the expression of autophagy-related proteins, Beclin1 and LC3, in TSCC.
- To determine the correlation between autophagy protein expression and clinicopathological features of TSCC.
- To elucidate the functional impact of autophagy modulation on TSCC cell behavior.
Main Methods:
- Immunohistochemistry was used to assess Beclin1 and LC3 expression in 50 TSCC samples.
- In vitro studies involved treating TSCC cells with autophagy modulators (rapamycin and 3-MA).
- Techniques including qPCR, Western blot, immunofluorescence, transmission electron microscopy, MTT assay, flow cytometry, wound healing, and transwell assays were employed.
Main Results:
- Down-regulation of Beclin1 and LC3 was frequently observed in TSCC.
- Decreased Beclin1 expression correlated with advanced T stage, clinical stage, and poor differentiation.
- Rapamycin-induced autophagy suppressed TSCC cell proliferation, migration, and invasion, while 3-MA-induced autophagy inhibition promoted these processes.
Conclusions:
- Autophagy plays a significant role in the progression of tongue squamous cell carcinoma.
- Beclin1 and LC3 expression levels are potential biomarkers for TSCC.
- Targeting autophagy presents a promising therapeutic strategy for TSCC.
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