Related Experiment Video
Updated: Sep 23, 2025

11:44
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
7.7K
Atractylodin Induces Apoptosis and Inhibits the Migration of A549 Lung Cancer Cells by Regulating ROS-Mediated
Tong Zhang1, Shu-Mei Li2, Yan-Nan Li1
1College of Life Science & Technology, Heilongjiang Bayi Agricultural University, Daqing 163319, China.
Molecules (Basel, Switzerland)
|May 14, 2022
Summary
Atractylodin (ATR) inhibits lung cancer cell proliferation and migration. This natural compound induces apoptosis and cell cycle arrest in A549 cells by regulating key signaling pathways and increasing reactive oxygen species.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Atractylodin (ATR) exhibits anticancer properties, but its precise mechanism in lung cancer is not fully understood.
- Lung cancer remains a leading cause of cancer-related mortality worldwide, necessitating novel therapeutic strategies.
Purpose of the Study:
- To investigate the inhibitory effects of ATR on A549 human lung cancer cells.
- To elucidate the molecular mechanisms underlying ATR's action in lung cancer.
Main Methods:
- Cell viability was assessed using the Cell Counting Kit-8 assay.
- Apoptosis, mitochondrial membrane potential, and reactive oxygen species (ROS) levels were analyzed via flow cytometry.
- Western blotting was employed to examine the regulation of key signaling pathways, including MAPK, STAT3, NF-κB, AKT, and Wnt.
Main Results:
- ATR significantly inhibited A549 cell proliferation and migration.
- ATR induced apoptosis and cell cycle arrest, which was linked to intracellular ROS accumulation.
- ATR modulated apoptosis through the MAPK, STAT3, and NF-κB pathways, and affected cell cycle and migration via the AKT and Wnt pathways, respectively.
Conclusions:
- ATR demonstrates significant potential as an anticancer agent against lung cancer.
- ATR exerts its effects by inducing apoptosis, cell cycle arrest, and inhibiting migration through complex signaling pathway modulation.
Related Concept Videos
PI3K/mTOR/AKT Signaling Pathway
4.1K
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...
4.1K
The Extrinsic Apoptotic Pathway
6.7K
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
6.7K
mTOR Signaling and Cancer Progression
3.9K
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...
The mTOR pathway or the...
3.9K

