Related Experiment Video

Updated: Jan 14, 2026

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

19.1K

Mitomycin C Induces Autophagy in Human Tracheal Fibroblasts and Suppresses Their Growth

Jeong-Mi Kim1,2,3, Sungryeal Kim1, Eun-Jeong Jeon1,4

  • 1Department of Otorhinolaryngology-Head and Neck Surgery Inha University College of Medicine Incheon Republic of Korea.

Laryngoscope Investigative Otolaryngology
|October 20, 2025
PubMed
Abstract

Insights

Mitomycin C (MMC) reduces tracheal fibroblast growth via autophagy, sparing epithelial cells. This suggests MMC’s potential as a targeted antifibrotic therapy for tracheal stenosis.

Area of Science:

  • Cell Biology
  • Fibrosis Research
  • Drug Mechanisms

Background:

  • Mitomycin C (MMC) is used to prevent tracheal stenosis fibrosis.
  • Its exact cellular mechanisms, especially regarding autophagy and cytotoxicity, are not fully understood.

Purpose of the Study:

  • To investigate the cytotoxic and autophagic effects of MMC on human tracheal fibroblasts (hTF) and human bronchial/tracheal epithelial cells (hTEC).
  • To elucidate MMC's role in regulating fibrosis.

Main Methods:

  • hTF and hTEC were treated with varying MMC concentrations (0.01-1 μg/mL) over 24-72 hours.
  • Assessed cell proliferation, autophagy markers (LC3, ATG5, Rab7), and fibrosis markers (αSMA, cyclin D1).
  • Evaluated effects on cell migration and fibroblast-to-myofibroblast transition.

Main Results:

  • MMC partially reduced hTEC proliferation without inducing autophagy.
  • MMC significantly suppressed hTF proliferation and induced autophagy in a dose- and time-dependent manner.
  • MMC increased autophagy markers in hTF, decreased proliferation markers, and attenuated TGFβ-induced αSMA, indicating antifibrotic effects.

Conclusions:

  • MMC selectively suppresses human tracheal fibroblast proliferation through autophagy-mediated cell death, while sparing epithelial cells.
  • This selective action highlights MMC's potential as a targeted antifibrotic agent for tracheal stenosis.
  • Further research is warranted to optimize MMC application and understand its long-term effects on airway remodeling.
Keywords:
Mitomycin Cautophagybronchial/tracheal epithelial celltracheal fibroblasttracheal stenosis

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

11.4K
Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy07:40

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy

Published on: May 26, 2023

1.5K

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...
4.6K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
7.7K
Destabilization of Microtubules01:45

Destabilization of Microtubules

The destabilization of microtubules can occur during different stages of the microtubule lifecycle, such as nucleation or elongation. It can take place at either end of the microtubule or in the microtubule lattices as a whole. The lifespan of individual microtubules within a cell varies according to the cell type and stage of the cell cycle. During interphase, the lifespan of the microtubule is about 30 minutes, while during cell division, it is about 15 minutes. In axonal microtubules of...
3.5K
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...
5.1K
Drugs that Stabilize Microtubules01:15

Drugs that Stabilize Microtubules

Microtubules are dynamic structures that undergo cycles of catastrophe and rescue. The microtubules play a central role in cell division by forming the spindle apparatus for segregating the chromosomes. This makes them ideal targets for regulating dividing cells in tumors and malignant cancer cells. Microtubule stabilizing drugs help stabilize the microtubule formation and promote its polymerization. Paclitaxel was the first microtubule stabilizing agent used as anticancer drug in chemotherapy...
2.6K