Related Experiment Video

Updated: Aug 16, 2026

Analysis of the c-KIT Ligand Promoter Using Chromatin Immunoprecipitation
09:40

Analysis of the c-KIT Ligand Promoter Using Chromatin Immunoprecipitation

Published on: June 27, 2017

c-myc expression correlates with suppression of c-kit protooncogene expression in small cell lung cancer cell lines

H Plummer1, J Catlett, J Leftwich

  • 1Department of Medicine, Medical College of Virginia, Richmond.

Cancer Research
|September 15, 1993
PubMed

Insights

Small cell lung cancer cells coexpress c-kit and hemopoietic stem cell factor, suggesting an autocrine growth loop. Myc gene family members differentially regulate c-kit expression, impacting cancer cell properties.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Small cell lung cancer (SCLC) often exhibits autocrine growth loops.
  • The c-kit protooncogene tyrosine kinase receptor and its ligand, hemopoietic stem cell factor, are implicated in cancer cell proliferation.

Purpose of the Study:

  • To investigate the coexpression of c-kit and its ligand in SCLC cell lines.
  • To determine the relationship between myc gene family expression and c-kit regulation in SCLC.

Main Methods:

  • Analysis of mRNA and protein levels of c-kit and hemopoietic stem cell factor in SCLC cell lines.
  • Transfection of SCLC cell lines with a c-myc expression vector.
  • Correlation analysis between the expression of c-kit, L-myc, N-myc, and c-myc genes.

Main Results:

  • Coexpression of c-kit and hemopoietic stem cell factor mRNA was observed in most SCLC cell lines, indicating a potential autocrine loop.
  • SCLC cell lines expressing c-kit also expressed either L-myc or N-myc, but not c-myc.
  • Heterologous expression of c-myc led to significant down-regulation of c-kit expression.

Conclusions:

  • The myc gene family, particularly c-myc, plays a role in regulating c-kit expression in SCLC.
  • Differential regulation of c-kit by N-myc/L-myc versus c-myc may contribute to distinct biological behaviors of SCLC tumors.

More Related Videos

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis11:44

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

Related Concept Videos

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...
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...
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 daughter...
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...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...