Does the undifferentiated PC12 cell line in terms of chromosome characteristics, proliferation, and drug reactions have the characteristics of cancer cells?
Where is it possible to acquire the pc12 gene profile to compare it with differentiated type?
And since we use it as a model of neurons in the study, how do we know if changes in the gene expression are related to cancerous features or neuronal characteristics? The details in the articles puzzled me a little bit.
For example, is it possible that the induction of growth in these cells by a drug is because the drug triggers cancer cell growth? Or is the activation of apoptosis by a drug attributable to the drug's anti-cancer effect?
PC 12 represent a cancer cell line in terms of proliferation but its chromosomal characteristics are not well established and may fluctuate from one clone to another. We have attempted long ago to characterize the chromosomal number of our PC 12 line but we can't obtain a clear pattern, even after isolation of clones by limit dilution. It only represents a model (neuronal-like) line which responds to NGF or FGF by transformation into cells with prolongements and dendrites. Some of the PC 12 clones secrete dopamine but not all of them.
It seems to me that HT 22 mouse cell line is probably more stable
2., 3. To compare the gene profile in PC12 cells please see this article.
Article Analysis of Gene Expression and Neuronal Phenotype in Neuros...
Figure 2:
Analysis of transcription patterns of neuronal genes.
Figure 3:
Evaluation of neuronal protein expression in differentiated NS-1 and PC12 cells by immunoblot analyses.
4. Of course, if a drug acts on cells and cell proliferation or apoptosis is observed, it means that the drug activates or inhibits certain receptors, signal transduction proteins (pathways) through which transcription factors and genes are activated or inhibited. The result of this entire chain of events is the activation of cell proliferation and apoptosis, depending on the nature of the drug, exposure conditions, activation or inhibition of specific proteins (cascades). For example, the binding of nerve growth factor (NGF) to the p75 receptor triggers the activation of JNK pathway, which induces the initiation of apoptosis, and activation BDNF through TrkA, TrkB causes cell proliferation.