Limits...
Eukaryotic cell encystation and cancer cell dormancy: is a greater devil veiled in the details of a lesser evil?

Baig AM, Khan NA, Abbas F - Cancer Biol Med (2015)

Bottom Line: These dormant cells veil themselves from detection by imaging and/or using biomarkers, which imposes an additional problem in targeting such cells.A similar form of hibernation process known as encystation is studied in detail for pathogenic unicellular eukaryotic microorganisms.We propose a strategy to induce dormancy and exit this state by application of knowledge gained from the encystation induction and retrieval processes in pathogenic eukaryotic microorganisms.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological and Biomedical Sciences, Aga Khan University, Karachi 75300, Pakistan.

ABSTRACT
Cancer cell dormancy is the main cause of cancer recurrence and failure of therapy as dormant cells evade not only the anticancer drugs but also the host immune system. These dormant cells veil themselves from detection by imaging and/or using biomarkers, which imposes an additional problem in targeting such cells. A similar form of hibernation process known as encystation is studied in detail for pathogenic unicellular eukaryotic microorganisms. By examination using microarray gene expression profiles, immunocytochemistry tools, and siRNAs during the process of encystation, understanding the covert features of cancer cell dormancy as proposed could be possible. This knowledge can be extended to dormant cancer cells to uncover the mechanisms that underlie this ghost, yet dangerous state of human cancers. We propose a strategy to induce dormancy and exit this state by application of knowledge gained from the encystation induction and retrieval processes in pathogenic eukaryotic microorganisms. Given that early detection and characterization of dormant malignant tumor cells is important as a general strategy to monitor and prevent the development of overt metastatic disease, this homology may enable the design of therapies that could either awake the dormant cell from dormancy to make it available for therapies or prolong such a phase to make cancer appear as a chronic disease.

No MeSH data available.


Related in: MedlinePlus

Row of LNCaP (above) and PC3 (below). (A) Induction of dormancy by the same stimuli that provoke encystation in Eukaryotic cells; (B) Cancer cells undergoing dormancy; (C) Dormant state established; (D) Revival from dormancy, by the same stimuli that cause excystation in eukaryotic cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4383842&req=5

f3: Row of LNCaP (above) and PC3 (below). (A) Induction of dormancy by the same stimuli that provoke encystation in Eukaryotic cells; (B) Cancer cells undergoing dormancy; (C) Dormant state established; (D) Revival from dormancy, by the same stimuli that cause excystation in eukaryotic cells.

Mentions: Substantial work has been conducted on encystation and excystation in unicellular eukaryotes2 like Acanthamoeba spp., Entamoeba, and Giardia. These eukaryotes can be tested for the presence of the aforementioned MOTHER features. Moreover, in-depth studies could be conducted to understand the MOTHER features fully. Recently, the Food and Drug Administration-approved drugs that target cell surface muscarinic (CHRM) G-protein coupled receptors (GPCRs) as antagonists3 have prevented these model eukaryotes from initiating the dormant state by blocking cyclic adenosine monophosphate-dependent and calcium-dependent pumps4. If tested in an in vitro prostate cancer cell model for dormancy, the identical GPCRs antagonists could provide clues to these hibernating mechanisms (Figure 3). These findings can be extended to experiments to first induce dormancy and then attempt to awaken cancer cells from that state in animal models. This search of homology in between encystation and dormancy aims to utilize these mechanisms for the two following purposes:


Eukaryotic cell encystation and cancer cell dormancy: is a greater devil veiled in the details of a lesser evil?

Baig AM, Khan NA, Abbas F - Cancer Biol Med (2015)

Row of LNCaP (above) and PC3 (below). (A) Induction of dormancy by the same stimuli that provoke encystation in Eukaryotic cells; (B) Cancer cells undergoing dormancy; (C) Dormant state established; (D) Revival from dormancy, by the same stimuli that cause excystation in eukaryotic cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4383842&req=5

f3: Row of LNCaP (above) and PC3 (below). (A) Induction of dormancy by the same stimuli that provoke encystation in Eukaryotic cells; (B) Cancer cells undergoing dormancy; (C) Dormant state established; (D) Revival from dormancy, by the same stimuli that cause excystation in eukaryotic cells.
Mentions: Substantial work has been conducted on encystation and excystation in unicellular eukaryotes2 like Acanthamoeba spp., Entamoeba, and Giardia. These eukaryotes can be tested for the presence of the aforementioned MOTHER features. Moreover, in-depth studies could be conducted to understand the MOTHER features fully. Recently, the Food and Drug Administration-approved drugs that target cell surface muscarinic (CHRM) G-protein coupled receptors (GPCRs) as antagonists3 have prevented these model eukaryotes from initiating the dormant state by blocking cyclic adenosine monophosphate-dependent and calcium-dependent pumps4. If tested in an in vitro prostate cancer cell model for dormancy, the identical GPCRs antagonists could provide clues to these hibernating mechanisms (Figure 3). These findings can be extended to experiments to first induce dormancy and then attempt to awaken cancer cells from that state in animal models. This search of homology in between encystation and dormancy aims to utilize these mechanisms for the two following purposes:

Bottom Line: These dormant cells veil themselves from detection by imaging and/or using biomarkers, which imposes an additional problem in targeting such cells.A similar form of hibernation process known as encystation is studied in detail for pathogenic unicellular eukaryotic microorganisms.We propose a strategy to induce dormancy and exit this state by application of knowledge gained from the encystation induction and retrieval processes in pathogenic eukaryotic microorganisms.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological and Biomedical Sciences, Aga Khan University, Karachi 75300, Pakistan.

ABSTRACT
Cancer cell dormancy is the main cause of cancer recurrence and failure of therapy as dormant cells evade not only the anticancer drugs but also the host immune system. These dormant cells veil themselves from detection by imaging and/or using biomarkers, which imposes an additional problem in targeting such cells. A similar form of hibernation process known as encystation is studied in detail for pathogenic unicellular eukaryotic microorganisms. By examination using microarray gene expression profiles, immunocytochemistry tools, and siRNAs during the process of encystation, understanding the covert features of cancer cell dormancy as proposed could be possible. This knowledge can be extended to dormant cancer cells to uncover the mechanisms that underlie this ghost, yet dangerous state of human cancers. We propose a strategy to induce dormancy and exit this state by application of knowledge gained from the encystation induction and retrieval processes in pathogenic eukaryotic microorganisms. Given that early detection and characterization of dormant malignant tumor cells is important as a general strategy to monitor and prevent the development of overt metastatic disease, this homology may enable the design of therapies that could either awake the dormant cell from dormancy to make it available for therapies or prolong such a phase to make cancer appear as a chronic disease.

No MeSH data available.


Related in: MedlinePlus