Related Experiment Video

Updated: Nov 18, 2025

Author Spotlight: A Selective Luciferase-Based Assay for Monitoring ATG4B 27 Activity in Cells
09:51

Author Spotlight: A Selective Luciferase-Based Assay for Monitoring ATG4B 27 Activity in Cells

Published on: June 30, 2023

1.2K

Chaperone-mediated autophagy affects tumor cell proliferation and cisplatin resistance in esophageal squamous cell

Dujuan Cao1, Danyang Shan1, Wenli Yan1

  • 1National Center for International Research in Cell and Gene Therapy, Sino-British Research Centre for Molecular Oncology, School of Basic Medical Sciences, Academy of Medical Sciences, Zhengzhou University, Zhengzhou, China.

Thoracic Cancer
|February 10, 2021
PubMed
Abstract

Insights

Down-regulating chaperone-mediated autophagy (CMA) by targeting LAMP2a inhibits esophageal squamous cell carcinoma (ESCC) progression and enhances cisplatin sensitivity, offering a new therapeutic strategy.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Biology

Background:

  • Chaperone-mediated autophagy (CMA) is a key lysosomal degradation pathway.
  • Lysosomal membrane associated protein 2a (LAMP2a) is the receptor for CMA and regulates its activity.
  • LAMP2a expression is linked to advanced tumor node metastasis (TNM) stages and poor survival in esophageal squamous cell carcinoma (ESCC), but the mechanism is unclear.

Purpose of the Study:

  • To investigate the role of CMA activity in human ESCC.
  • To explore the potential of modulating CMA as a therapeutic strategy for ESCC.

Main Methods:

  • Modulation of CMA activity using LAMP2a manipulation or small molecular compounds in human ESCC cells.
  • Assessment of ESCC cell proliferation and colony formation.
  • Evaluation of ESCC cell sensitivity to cisplatin.

Main Results:

  • Down-regulating CMA activity inhibited ESCC cell proliferation and colony formation.
  • Reduced CMA activity increased the sensitivity of ESCC cells to cisplatin.
  • LAMP2a downregulation emerged as a potential therapeutic approach.

Conclusions:

  • CMA plays a significant role in the progression of human ESCC.
  • Targeting CMA by down-regulating LAMP2a presents a promising therapeutic strategy for ESCC treatment.
  • Further research into CMA modulation could lead to novel anti-cancer therapies for ESCC.
Keywords:
cell proliferationchaperone-mediated autophagycisplatin resistanceesophageal squamous cell carcinomalysosomal membrane associated protein 2a

More Related Videos

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics06:00

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

11.3K
Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo09:19

Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo

Published on: February 6, 2015

8.9K

Related Concept Videos

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...
4.9K
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,...
5.3K
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...
4.1K
Delivery Pathways to the Lysosome01:36

Delivery Pathways to the Lysosome

Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
Endocytosis
In endocytosis, the cell membrane takes up macromolecules and particles from the surrounding medium. Clathrin-mediated...
8.4K
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
8.1K
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
9.7K