Related Experiment Video

Updated: May 29, 2025

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
09:29

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies

Published on: September 30, 2016

13.6K

Antitumor Effects of Tryptanthrin on Colorectal Cancer by Regulating the Mitogen-Activated Protein Kinase Signaling

Simeng Lu1, Bao-Long Hou1, Ting Wang1

  • 1Co-construction Collaborative Innovation Center of Chinese Medicine Resources Industrialization by Shaanxi & Education Ministry, State Key Laboratory of Research & Development of Characteristic Qin Medicine Resources (Cultivation), Shaanxi University of Chinese Medicine, Xianyang, Shaanxi712046, China.

ACS Omega
|February 3, 2025
PubMed

Insights

Tryptanthrin (TRYP) inhibits colorectal cancer (CRC) by inducing apoptosis and cell cycle arrest. This study reveals TRYP targets topoisomerase I (Topo I) and indole amine 2,3-dioxygenase 1 (IDO1), offering a basis for CRC drug development.

Area of Science:

  • Pharmacology
  • Oncology
  • Molecular Biology

Background:

  • Tryptanthrin (TRYP), an indole quinazoline alkaloid, exhibits diverse pharmaceutical activities.
  • The precise mechanisms of TRYP's action against colorectal cancer (CRC) are not fully understood.

Purpose of the Study:

  • To investigate the antitumor effects of TRYP on CRC models in vitro and in vivo.
  • To elucidate the molecular mechanisms underlying TRYP's anti-CRC activity.

Main Methods:

  • In vitro assays: cell proliferation, migration, cell cycle analysis, apoptosis assays (Western blotting for Bax, Bcl-2, cleaved caspase 3).
  • Transcriptome sequencing and Western blotting to analyze signaling pathways (MAPK pathway, p-Erk, p-p38, p-Jnk).
  • In vivo studies: tumor growth inhibition in mice, histological analysis (Ki67), apoptosis assessment.

Main Results:

  • TRYP inhibited SW620 cell proliferation and migration, induced S-phase arrest and apoptosis, and modulated apoptosis-related proteins (Bax, Bcl-2, cleaved caspase 3).
  • TRYP affected the MAPK signaling pathway by altering p-Erk, p-p38, and p-Jnk expression.
  • TRYP directly targeted topoisomerase I (Topo I) and indole amine 2,3-dioxygenase 1 (IDO1), inhibiting tumor growth and inducing apoptosis in vivo.

Conclusions:

  • TRYP demonstrates significant antitumor effects against CRC through apoptosis induction and cell cycle arrest.
  • The mechanisms involve the inhibition of Topo I and IDO1, and regulation of the MAPK signaling pathway.
  • This study provides the first evidence of TRYP directly inhibiting Topo I, establishing a scientific foundation for its therapeutic potential in CRC.

More Related Videos

Network Pharmacology Prediction and Experimental Validation of Trichosanthes-Fritillaria thunbergii Action Mechanism Against Lung Adenocarcinoma13:18

Network Pharmacology Prediction and Experimental Validation of Trichosanthes-Fritillaria thunbergii Action Mechanism Against Lung Adenocarcinoma

Published on: March 3, 2023

1.2K
Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 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...
3.7K
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...
7.4K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.6K
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...
2.0K
Drugs that Destabilize Microtubules01:10

Drugs that Destabilize Microtubules

Microtubules are dynamic structures and can be regulated by microtubule targeting agents (MTAs). Microtubule destabilizing drugs are a class of MTAs that destabilize and prevent microtubules' polymerization. Both natural and synthetic chemicals can be found under this class of drugs. Vincristine and vinblastine, two vinca alkaloids, and colchicine were among the first to be discovered. These drugs can affect cells in various ways, either by inducing a change in cell morphology, preventing...
1.9K
The Tumor Microenvironment02:17

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
6.5K