Related Experiment Video

Updated: Nov 18, 2025

Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis
07:26

Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis

Published on: January 31, 2025

788

[NCTD Retards AML HL60 Cell Proliferation via Targeting Hedgehog/SOX2 axis]

Ming-Yan Fu1, Wei-Wei Chen1, Na Gao1

  • 1Department of Hematology, Cancer Research Institute, Binzhou Medical University Hospital, Binzhou 256600, Shandong Province, China.

Zhongguo Shi Yan Xue Ye Xue Za Zhi
|February 8, 2021
PubMed
Abstract

Insights

Norcantharidin (NCTD) inhibits leukemia cell growth by targeting the Hedgehog/SOX2 pathway. This compound reduces proliferation and affects key regulators like SMO and GLI1 in leukemia cells.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • The sonic Hedgehog (SHH) pathway plays a role in cell proliferation and is implicated in various cancers, including leukemia.
  • SOX2 is a transcription factor downstream of the SHH pathway, often overexpressed in cancers.
  • Norcantharidin (NCTD) is a derivative of cantharidin with potential anti-cancer properties.

Purpose of the Study:

  • To investigate the effect of norcantharidin (NCTD) on leukemia cell proliferation.
  • To determine if NCTD disrupts the sonic Hedgehog (SHH) pathway and its downstream target SOX2.
  • To explore the role of the SHH/SOX2 axis in NCTD's anti-leukemic activity.

Main Methods:

  • Cell Counting Kit-8 (CCK8) assays were used to assess the proliferation of HL60 and NB4 leukemia cells.
  • Western blotting was employed to detect protein expression levels of SMO, GLI1, and SOX2 after NCTD treatment.
  • HL60 cells were genetically modified to overexpress GLI1 or SOX2 to study their impact on proliferation and NCTD resistance.

Main Results:

  • NCTD and inhibitors of SMO/GLI1 significantly inhibited HL60 and NB4 cell proliferation in a dose-dependent manner.
  • NCTD treatment led to a remarkable decrease in the protein levels of SMO, GLI1, and SOX2 in HL60 cells.
  • Overexpression of GLI1 or SOX2 in HL60 cells conferred a proliferative advantage and increased resistance to NCTD treatment.

Conclusions:

  • Norcantharidin (NCTD) effectively attenuates leukemia cell proliferation.
  • NCTD exerts its anti-leukemic effect by targeting the Hedgehog/SOX2 signaling axis.
  • The SHH/SOX2 pathway is a critical regulator of leukemia cell growth and response to NCTD.

More Related Videos

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics06:00

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

Published on: May 14, 2016

11.3K
Isolation, Enrichment, and Maintenance of Medulloblastoma Stem Cells06:32

Isolation, Enrichment, and Maintenance of Medulloblastoma Stem Cells

Published on: September 1, 2010

16.6K

Related Concept Videos

Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
8.1K
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
2.3K
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...
4.9K
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...
5.3K
Notch Signaling Pathway03:14

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
4.8K