Related Experiment Video

Updated: Jul 29, 2025

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

1.6K

Rhein Induces Oral Cancer Cell Apoptosis and ROS via Suppresse AKT/mTOR Signaling Pathway In Vitro and In Vivo

Haibo Zhang1,2,3, Lei Ma1,2, Eungyung Kim1,2

  • 1Department of Animal Science and Biotechnology, Kyungpook National University, Sangju 37224, Republic of Korea.

International Journal of Molecular Sciences
|May 27, 2023
PubMed

Insights

Rhein, a natural compound, effectively inhibits oral cancer growth by inducing apoptosis and cell cycle arrest. It also reduces migration and invasion by targeting key proteins and the AKT/mTOR pathway, showing potential as an oral cancer therapeutic.

Area of Science:

  • Oncology
  • Natural Products Chemistry
  • Molecular Biology

Background:

  • Oral cancer presents a significant global health challenge with high mortality rates.
  • Rhein, a compound from rhubarb, shows promise in cancer therapy, but its role in oral cancer requires elucidation.

Purpose of the Study:

  • To investigate the anticancer effects of rhein on oral cancer cells.
  • To explore the underlying molecular mechanisms of rhein's action in oral cancer.

Main Methods:

  • Cell proliferation, soft agar colony formation, migration, and invasion assays were used to assess anti-growth effects.
  • Flow cytometry analyzed cell cycle and apoptosis, while immunoblotting explored molecular mechanisms.
  • In vivo efficacy was evaluated using oral cancer xenograft models.

Main Results:

  • Rhein significantly inhibited oral cancer cell growth, inducing apoptosis and S-phase cell cycle arrest.
  • Rhein suppressed oral cancer cell migration and invasion by modulating epithelial-mesenchymal transition (EMT) proteins.
  • Rhein promoted reactive oxygen species (ROS) accumulation, inhibiting the AKT/mTOR signaling pathway.

Conclusions:

  • Rhein demonstrates potent in vitro and in vivo anticancer activity against oral cancer.
  • The mechanism involves inducing apoptosis and ROS via the AKT/mTOR pathway, leading to cell cycle arrest.
  • Rhein is a promising therapeutic candidate for oral cancer treatment.
Keywords:
apoptosisautophagymTORoral cancerrhein

More Related Videos

Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma10:21

Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma

Published on: September 20, 2024

499
Radiation Treatment of Organotypic Cultures from Submandibular and Parotid Salivary Glands Models Key In Vivo Characteristics07:38

Radiation Treatment of Organotypic Cultures from Submandibular and Parotid Salivary Glands Models Key In Vivo Characteristics

Published on: May 17, 2019

8.2K

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...
3.8K
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...
3.7K
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...
4.6K
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
4.0K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
5.7K
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...
9.0K