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PML Surfs into HIPPO Tumor Suppressor Pathway.

Strano S, Fausti F, Di Agostino S, Sudol M, Blandino G - Front Oncol (2013)

Bottom Line: Growth arrest, inhibition of cell proliferation, apoptosis, senescence, and differentiation are the most characterized effects of a given tumor suppressor response.The latter may happen through the concomitant involvement of common nodal proteins.PML, in addition to its own anti-tumor activity, contributes to the assembly of an integrated and superior network that may be necessary for the maximization of the tumor suppressor response to diverse oncogenic insults.

View Article: PubMed Central - PubMed

Affiliation: Molecular Chemoprevention Group, Molecular Medicine Area, Regina Elena National Cancer Institute Rome, Italy.

ABSTRACT
Growth arrest, inhibition of cell proliferation, apoptosis, senescence, and differentiation are the most characterized effects of a given tumor suppressor response. It is becoming increasingly clear that tumor suppression results from the integrated and synergistic activities of different pathways. This implies that tumor suppression includes linear, as well as lateral, crosstalk signaling. The latter may happen through the concomitant involvement of common nodal proteins. Here, we discuss the role of Promyelocytic leukemia protein (PML) in functional cross-talks with the HIPPO and the p53 family tumor suppressor pathways. PML, in addition to its own anti-tumor activity, contributes to the assembly of an integrated and superior network that may be necessary for the maximization of the tumor suppressor response to diverse oncogenic insults.

No MeSH data available.


Related in: MedlinePlus

Central role of YAP in proliferation inhibiting pathways. Schematic representation of the central role of YAP in inducing the inhibition of proliferation, by integrating and mediating different upstream stimuli. It was shown that RASSF1A disrupts the inhibitory complex between RAF1 and MST2 and favors the physical association between MST2 and LATS1 concomitantly; therefore, leading to YAP1 phosphorylation and nuclear re-localization where it binds to p73 and potentiates its apoptotic activity. Oncogenic transformation as well as DNA damage (achieved by CDDP treatment) leads to YAP accumulation and to its functional activation.
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Figure 3: Central role of YAP in proliferation inhibiting pathways. Schematic representation of the central role of YAP in inducing the inhibition of proliferation, by integrating and mediating different upstream stimuli. It was shown that RASSF1A disrupts the inhibitory complex between RAF1 and MST2 and favors the physical association between MST2 and LATS1 concomitantly; therefore, leading to YAP1 phosphorylation and nuclear re-localization where it binds to p73 and potentiates its apoptotic activity. Oncogenic transformation as well as DNA damage (achieved by CDDP treatment) leads to YAP accumulation and to its functional activation.

Mentions: In fact PML, YAP, and p73 can be recruited on Bax and p53AIP1 apoptotic gene promoters, which contain p73 binding sites within their promoter regions, in response to CDDP and PML binds to its own promoter and first intron where YAP and p73 were also recruited, and promotes its own transcriptional activation (Figure 3).


PML Surfs into HIPPO Tumor Suppressor Pathway.

Strano S, Fausti F, Di Agostino S, Sudol M, Blandino G - Front Oncol (2013)

Central role of YAP in proliferation inhibiting pathways. Schematic representation of the central role of YAP in inducing the inhibition of proliferation, by integrating and mediating different upstream stimuli. It was shown that RASSF1A disrupts the inhibitory complex between RAF1 and MST2 and favors the physical association between MST2 and LATS1 concomitantly; therefore, leading to YAP1 phosphorylation and nuclear re-localization where it binds to p73 and potentiates its apoptotic activity. Oncogenic transformation as well as DNA damage (achieved by CDDP treatment) leads to YAP accumulation and to its functional activation.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3585432&req=5

Figure 3: Central role of YAP in proliferation inhibiting pathways. Schematic representation of the central role of YAP in inducing the inhibition of proliferation, by integrating and mediating different upstream stimuli. It was shown that RASSF1A disrupts the inhibitory complex between RAF1 and MST2 and favors the physical association between MST2 and LATS1 concomitantly; therefore, leading to YAP1 phosphorylation and nuclear re-localization where it binds to p73 and potentiates its apoptotic activity. Oncogenic transformation as well as DNA damage (achieved by CDDP treatment) leads to YAP accumulation and to its functional activation.
Mentions: In fact PML, YAP, and p73 can be recruited on Bax and p53AIP1 apoptotic gene promoters, which contain p73 binding sites within their promoter regions, in response to CDDP and PML binds to its own promoter and first intron where YAP and p73 were also recruited, and promotes its own transcriptional activation (Figure 3).

Bottom Line: Growth arrest, inhibition of cell proliferation, apoptosis, senescence, and differentiation are the most characterized effects of a given tumor suppressor response.The latter may happen through the concomitant involvement of common nodal proteins.PML, in addition to its own anti-tumor activity, contributes to the assembly of an integrated and superior network that may be necessary for the maximization of the tumor suppressor response to diverse oncogenic insults.

View Article: PubMed Central - PubMed

Affiliation: Molecular Chemoprevention Group, Molecular Medicine Area, Regina Elena National Cancer Institute Rome, Italy.

ABSTRACT
Growth arrest, inhibition of cell proliferation, apoptosis, senescence, and differentiation are the most characterized effects of a given tumor suppressor response. It is becoming increasingly clear that tumor suppression results from the integrated and synergistic activities of different pathways. This implies that tumor suppression includes linear, as well as lateral, crosstalk signaling. The latter may happen through the concomitant involvement of common nodal proteins. Here, we discuss the role of Promyelocytic leukemia protein (PML) in functional cross-talks with the HIPPO and the p53 family tumor suppressor pathways. PML, in addition to its own anti-tumor activity, contributes to the assembly of an integrated and superior network that may be necessary for the maximization of the tumor suppressor response to diverse oncogenic insults.

No MeSH data available.


Related in: MedlinePlus