A comparison between malignant and aging cells shows that cancer cells do not age, can proliferate without limits, show increased metabolism.
As a result, cancer cells supplant senescent cells.
Thus, cancer manifests itself as local uncontrolled "rejuvenation" in an organism.
The metabolic, proliferative, and growth characteristics of the cancer cells are the opposite of those observed in cellular aging (both replicative and functional).
Indeed, cancer cells are potentially immortal (due to avoiding apoptosis), while aging cells (both proliferating and postmitotic) normally die via apoptosis.
Cancer cells can proliferate to an unlimited extent.
Aging proliferating cells however, exhibit a decline in proliferative ability with each cell division and finally suffer irreversible growth arrest (also called replicative senescence).
Whereas cancer cells are de-differentiating, the final stage of normal cellular development is terminal differentiation.
Cancer cells often have an increased metabolism, while functionally aging cells (e.g., postmitotic neurons) decline in metabolic activity.
Cancer cells may secrete factors that increase blood supply, and produce embryonic proteins, such as α-fetoprotein, while aging cells do not.
Many of these cancer features are inherent to most "young" cells in an organism, that is, embryonic cells.
Embryonic cells proliferate vigorously, are capable of extensive migration, secrete factors that increase the local supply of blood, and produce enzymes capable of degrading basement membranes.
Thus, cancer and aging are in many instances opposite phenotypic conditions.
One might even say that cancer manifests itself as local and uncontrolled "rejuvenescence" in an organism.
Understanding the mechanisms creating such "antiaging" condition in an aging organism may help in developing both antiaging and anticancer interventions.
Recent evidence suggests that cancer and aging share common genes, which are oppositely expressed, however.
These are proto-oncogenes and tumor suppressors.
They normally contribute to apoptosis/growth arrest and growth signal transduction pathways in the cell.
The proto-oncogenes are down regulated In aging cells, while in cancer cells they are over expressed.
Tumor suppressors are permanently expressed In aging cells, while in cancer cells they are down regulated.
It is proposed is that controlled "cancer like" expression of some of these genes may have an anti-aging effect on cells and organisms.
The comparative analysis shows that phenotypes of cancer and aging are in many instances contrary.
Cancer cells do not "age"; their metabolic, proliferative, and growth characteristics are opposite to those observed In cellular aging (both replicative and functional).
That is, cancer manifests itself as local uncontrolled "rejuvenation" in an organism.
Available data suggest that the opposite phenotypic features of aging and cancer arise from the opposite regulation of common signaling pathways such as apoptosis/growth arrest and growth signal transduction pathways.
Genes normally managing cellular aging promote cancer when contrarily expressed.
Signaling pathways oppositely manifested in cancer and aging
|Apoptosis / growth arrest
||In cancer cells
||In aging cells
||In aging organism
||Induces apoptosis / growth arrest
|Downregulated in most human cancers (Soussi, 2000; Hickman, 2002)
||Elevated expression (Kulju and Lehman; Antropova et al., 2002)
||Upregulating mutation is associated with early aging phenotype and lower cancer risk in mice (Donehower)
||"Death" receptor of apoptotic signal
||Decreased expression (Pinkoski and Green, 2000)
||Higher expression on cells from adults compared with newboms (Miyawaki et at., 1992)
||Proportion of cells expressing CD95 is higher in older individuals (Aggarwal and Gupta)
|Overexpressed in some cancers (Ross, 1997)
||Decreased levels (Miyashita et at., 1994; Peters and Vousden)
||Decreased expression in lymphocytes from older individuals (Aggarwal and Gupta)
|Growth signal transduction
||In cancer cells
||In aging cells
||In aging organism
|Overexpressed in many cancers (Peters and Vousden)
||Decreased expression in senescent cells (Dean et al., 1986; Peters and Vousden)
||Sustained expression of the myc rescued rat embryo cells from senescence (Schwab and Bishop, 1988)
|Activated in some cancers (Frame and Balmain, 2000)
||Decreased expression in senescent cells (Delgado et al., 1986)
||Activity is lower in old rats (Pahlavani and Vargas, 2000).
Controlled expression extends the reproductive life span in yeast (Jazwinski et al.)
|Tyrosine kinase receptors
||Growth factor receptors (e.g., erb-B, TRK)
|Overexpressed in some cancers (Peters and Vousden)
||Receptor density and mitogenic response decrease with donor age (Recnstra et al., 1996; DeKeyser et al., 1994; Hou et al., 2002)
||Overexpression of tkr-1 increases longevity and stress-resistance in nematodes (Murakami and Johnson)
This finding may help to developing new antiaging and anticancer interventions.
First, the controlled activation of oncogenes or the down regulation of tumor suppressors might produce an antiaging effect on cells and (possibly) on an organism.
The latter, however, needs careful investigation.
Second, the fact that cancer cells do not "age" suggests that these cells may have a survival advantage in the surrounding senescent cells.
Cancer risk could increase with age, partly because the proportion of the senescent cells increases in the aging organism.
In this situation, the rejuvenation of normal host cells surrounding the tumor could be a perspective anticancer treatment.
For instance, grafting young proliferating cells (such as embryonic/stem cells) in the area of a malignant tumor might help to supplant cancer cells rather than to kill them.