Related Experiment Video

Updated: Mar 28, 2026

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
11:13

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

Published on: June 9, 2023

2.5K

Juglanthraquinone C Induces Intracellular ROS Increase and Apoptosis by Activating the Akt/Foxo Signal Pathway in HCC

Ya-Qin Hou1, Yao Yao2, Yong-Li Bao3

  • 1National Engineering Laboratory for Druggable Gene and Protein Screening, Northeast Normal University, Changchun 130024, China ; Research Center of Agriculture and Medicine Gene Engineering of Ministry of Education, Northeast Normal University, Changchun 130024, China ; Institute of Genetics and Cytology, Northeast Normal University, Changchun 130024, China.

Oxidative Medicine and Cellular Longevity
|December 19, 2015
PubMed

Insights

Juglanthraquinone C induces cancer cell death by activating the Akt/Foxo pathway and increasing reactive oxygen species (ROS). This natural compound shows promise for hepatocellular carcinoma (HCC) treatment.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pharmacology

Background:

  • Naturally occurring anthraquinones, like Juglanthraquinone C (JC) from Juglans mandshurica, exhibit anticancer properties.
  • Understanding the precise molecular mechanisms of JC-induced apoptosis is crucial for its therapeutic development.

Purpose of the Study:

  • To elucidate the detailed cytotoxicity mechanism of Juglanthraquinone C (JC) in hepatocellular carcinoma (HCC) cell lines (HepG2 and BEL-7402).
  • To investigate the role of the Akt/Foxo signaling pathway and reactive oxygen species (ROS) in JC-induced apoptosis.

Main Methods:

  • Gene expression profiling using Affymetrix HG-U133 Plus 2.0 arrays.
  • Western blot analysis to assess protein activation and levels.
  • Manipulation of Akt and Foxo3a expression to determine their roles in apoptosis.
  • Measurement of intracellular ROS levels and assessment of antioxidant effects.

Main Results:

  • JC treatment induced apoptosis and hyperactivated the Akt signaling pathway in HCC cells.
  • Akt activation was essential for JC-induced apoptosis, while Foxo3a inactivation suppressed it.
  • JC suppressed Foxo3a nuclear localization, leading to increased intracellular ROS by inhibiting ROS scavenging enzymes.
  • Antioxidants N-acetyl-L-cysteine and catalase reduced JC-induced apoptosis.

Conclusions:

  • Juglanthraquinone C induces apoptosis in HCC cells through the activation of the Akt/Foxo signaling pathway.
  • JC-induced apoptosis is mediated by the inactivation of Foxo3a, resulting in increased intracellular ROS levels.
  • JC represents a potential therapeutic agent for HCC, targeting the Akt/Foxo pathway and ROS generation.

More Related Videos

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen19:44

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

19.3K

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...
5.1K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

1.7K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
9.2K
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...
6.3K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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...
9.3K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
13.9K