Related Experiment Video

Updated: May 28, 2025

A Combined 3D Tissue Engineered In Vitro/In Silico Lung Tumor Model for Predicting Drug Effectiveness in Specific Mutational Backgrounds
13:34

A Combined 3D Tissue Engineered In Vitro/In Silico Lung Tumor Model for Predicting Drug Effectiveness in Specific Mutational Backgrounds

Published on: April 6, 2016

10.1K

Jatrorrhizine Exhibits an Antitumor Effect Against Gefitinib-resistant Non-small Cell Lung Cancer via Inhibiting

Kainan Yao1, Zeli Li2, Gulizeba Muhetaer3

  • 1Shenzhen Bao'an Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, China.

Chemistry & Biodiversity
|February 9, 2025
PubMed

Insights

Jatrorrhizine shows potential in treating gefitinib-resistant non-small cell lung cancer (NSCLC) by inhibiting the PI3K/mTOR pathway. This natural compound suppresses tumor cell proliferation, migration, and invasion while promoting apoptosis.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Gefitinib resistance (GR) mediated by epidermal growth factor receptor (EGFR) mutations poses a significant challenge in non-small cell lung cancer (NSCLC) treatment.
  • Identifying novel therapeutic agents effective against resistant NSCLC is crucial.

Purpose of the Study:

  • To investigate the anti-cancer effects of jatrorrhizine on gefitinib-resistant NSCLC cells.
  • To elucidate the underlying molecular mechanism of jatrorrhizine's action, focusing on the PI3K/mTOR signaling pathway.

Main Methods:

  • Cell viability, migration, invasion, and apoptosis assays were performed on H1975 NSCLC cells treated with jatrorrhizine.
  • Bioinformatic analyses (Swiss Target Prediction, TCM Database, GeneCards, OMIM) and molecular docking were used to predict and verify drug targets.
  • Western blot analysis was employed to assess the impact of jatrorrhizine on the PI3K/mTOR signaling pathway.

Main Results:

  • Jatrorrhizine demonstrated significant anti-tumor activity, inhibiting proliferation and invasion while inducing apoptosis in H1975 cells.
  • The PI3K-Akt signaling pathway was identified as a critical target for jatrorrhizine's anti-NSCLC effects.
  • Western blot confirmed that jatrorrhizine down-regulates the phosphorylation of PI3K/mTOR in H1975 cells.

Conclusions:

  • Jatrorrhizine exhibits potent anti-cancer properties against gefitinib-resistant NSCLC.
  • Inhibition of the PI3K/mTOR signaling pathway is a key mechanism by which jatrorrhizine exerts its therapeutic effects.
  • Jatrorrhizine represents a promising novel compound for the treatment of resistant NSCLC.
Keywords:
gefitinib resistance | jatrorrhizine | mTOR | non‐small cell lung cancer | PI3K

More Related Videos

Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib09:38

Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib

Published on: June 26, 2019

7.9K
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

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
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
3.4K
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...
6.4K
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
Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers01:26

Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers

Receptor tyrosine kinase inhibitors (TKIs) and calcium channel blockers (CCBs) are two critical categories of drugs employed in the treatment of pulmonary artery hypertension (PAH). PAH is a disease that causes high blood pressure in the pulmonary arteries, resulting in chest pain, fatigue, and shortness of breath.
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
131