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Related Concept Videos

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
Autophagy01:27

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Tumor Progression02:07

Tumor Progression

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Delivery Pathways to the Lysosome

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Endocytosis
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Related Experiment Video

Updated: May 13, 2026

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy
07:20

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.

Journal of Oral Pathology & Medicine : Official Publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
|March 8, 2013
PubMed
Summary
This summary is machine-generated.

Autophagy, crucial for cell health, is often down-regulated in tongue squamous cell carcinoma (TSCC). Modulating autophagy impacts TSCC progression, suggesting its therapeutic potential.

Keywords:
Beclin1LC3autophagytongue squamous cell carcinoma

Related Experiment Videos

Last Updated: May 13, 2026

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy
07:20

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy

Published on: January 31, 2025

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.