Related Experiment Video
Updated: Dec 15, 2025

Genome-wide RNAi Screening to Identify Host Factors That Modulate Oncolytic Virus Therapy
Published on: April 3, 2018
Isorhamnetin induces the paraptotic cell death through ROS and the ERK/MAPK pathway in OSCC cells
Qian Chen1, Shaojuan Song1, Zhen Wang1
1State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Chinese Academy of Medical Sciences Research Unit of Oral Carcinogenesis and Management, Sichuan University, Chengdu, China.
Objective:
There were rarely investigations on the effects and molecular mechanisms of oral squamous cell carcinoma (OSCC) cells when treated with isorhamnetin. This article assesses the anti-cancer effect of isorhamnetin.
Methods And Materials:
Oral squamous cell carcinoma cells were treated with or without isorhamnetin. Cell proliferation, cell cycle arrest, cell migration, cell death, and the related signaling pathways were evaluated.
Results:
The results revealed that cell proliferation was inhibited in a dose- and time-dependent manner, which was confirmed by diminished cell viability and revealed by decreased in the number of cell colonies. In addition, the cell cycle arrested in the G2/M phase, and the protein levels of cyclin B1 and CDC2 were suppressed. Moreover, the cell migration was inhibited, and the protein levels of related proteins were modulated. Furthermore, it could be observed that abundant cytoplasmic vacuoles existed which that were derived from mitochondria and the endoplasmic reticulum. It was confirmed that cell death did not result from apoptosis and may have which may be apt to paraptosis. Isorhamnetin was observed to upregulate phosphorylated ERK cascades and increase intracellular reactive oxygen species levels.
Conclusions:
Our study suggested that the anti-cancer effect of isorhamnetin might trigger paraptosis, which may indicate a new therapeutic approach to OSCC.
Insights
Isorhamnetin effectively inhibits oral squamous cell carcinoma (OSCC) growth by inducing paraptosis, a distinct form of cell death. This finding suggests isorhamnetin as a potential therapeutic agent for OSCC treatment.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- Oral squamous cell carcinoma (OSCC) remains a significant health concern with limited therapeutic options.
- Investigating novel compounds like isorhamnetin for anti-cancer properties is crucial.
Purpose of the Study:
- To evaluate the anti-cancer effects of isorhamnetin on OSCC cells.
- To elucidate the molecular mechanisms underlying isorhamnetin's action.
Main Methods:
- OSCC cells were treated with isorhamnetin.
- Assessed were cell proliferation, cell cycle, migration, and cell death.
- Related signaling pathways, including ERK, were analyzed.
Main Results:
- Isorhamnetin inhibited OSCC cell proliferation and viability in a dose- and time-dependent manner.
- Cell cycle arrest at G2/M phase and suppressed cyclin B1/CDC2 levels were observed.
- Cell death occurred via paraptosis, characterized by cytoplasmic vacuoles, and was linked to upregulated p-ERK and increased ROS.
Conclusions:
- Isorhamnetin exhibits potent anti-cancer activity against OSCC.
- The mechanism involves inducing paraptosis, offering a novel therapeutic strategy.
- Further research into isorhamnetin for OSCC treatment is warranted.
Related Concept Videos
PI3K/mTOR/AKT Signaling Pathway
Overview of Cell Death
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
MAPK Signaling Cascades
Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
The Intrinsic Apoptotic Pathway

