Related Experiment Video

Updated: Oct 21, 2025

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
06:00

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

Published on: May 14, 2016

11.2K

Induction of G2/M Cell Cycle Arrest via p38/p21Waf1/Cip1-Dependent Signaling Pathway Activation by Bavachinin in

Jih-Tung Pai1, Ming-Wei Hsu2, Yann-Lii Leu3,4

  • 1Division of Hematology and Oncology, Tao-Yuan General Hospital, Ministry of Health and Welfare, Taoyuan City 33004, Taiwan.

Molecules (Basel, Switzerland)
|September 10, 2021
PubMed

Insights

Bavachinin, a compound from Traditional Chinese Medicine, effectively inhibits non-small-cell lung cancer (NSCLC) cell growth. It works by inducing G2/M cell cycle arrest through the p38 MAPK-mediated p21 pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Non-small-cell lung cancer (NSCLC) remains a leading cause of cancer mortality worldwide.
  • Despite advancements, improving NSCLC patient survival necessitates novel chemopreventive strategies.
  • Traditional Chinese Medicine (TCM) offers a promising source for safe and cost-effective cancer chemoprevention.

Purpose of the Study:

  • To evaluate the anti-cancer activity of bavachinin, a flavanone from *Proralea corylifolia* L., against NSCLC.
  • To elucidate the molecular mechanisms underlying bavachinin's anti-cancer effects in NSCLC cells.
  • To investigate the role of cell cycle regulation and specific signaling pathways in bavachinin's action.

Main Methods:

  • Assessed bavachinin's effect on NSCLC cell viability and colony formation in vitro.
  • Analyzed cell cycle progression, focusing on G2/M phase arrest.
  • Investigated the expression and interaction of key cell cycle regulators (e.g., p21, cyclin B, cdc2).
  • Examined the involvement of MAPK and AKT signaling pathways, particularly p38 MAPK.
  • Utilized gene silencing techniques to confirm the role of p21 in bavachinin's mechanism.

Main Results:

  • Bavachinin demonstrated a dose-dependent inhibition of NSCLC cell viability and colony formation.
  • The compound induced G2/M cell cycle arrest, suppressing key regulators like cyclin B and p-cdc2.
  • A significant upregulation of p21Waf1/Cip1 was observed, which was crucial for the G2/M arrest.
  • Bavachinin activated MAPK and AKT signaling pathways.
  • Inhibition of p38 MAPK reversed bavachinin-induced p21 expression and G2/M arrest, highlighting its critical role.

Conclusions:

  • Bavachinin exhibits potent anti-cancer activity against NSCLC cells.
  • The anti-cancer effects are mediated by G2/M cell cycle arrest, primarily through the p38 MAPK-dependent upregulation of p21Waf1/Cip1.
  • Bavachinin represents a potential therapeutic agent derived from TCM for NSCLC chemoprevention.
Keywords:
G2/M cell cycle arrestbavachininnon-small-cell lung cancer (NSCLC)p21Waf1/Cip1p38 MAPK

More Related Videos

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

27.8K
Analysis of Cell Cycle Position in Mammalian Cells12:19

Analysis of Cell Cycle Position in Mammalian Cells

Published on: January 21, 2012

60.8K

Related Concept Videos

Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
36.7K
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...
5.1K
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
9.6K
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...
7.1K
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...
4.7K
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...
7.2K