Zinc protoporphyrin suppresses cancer cell viability through a heme oxygenase-1-independent mechanism: the involvement of the Wnt/β-catenin signaling pathway.

Abstract:

:Zinc protoporphyrin (ZnPP), a known inhibitor of heme oxygenase-1 (HO-1), has been reported to have anticancer activity in both in vitro and in vivo model systems. While the mechanisms of ZnPP's anticancer activity remain to be elucidated, it is generally believed that ZnPP suppresses tumor growth through inhibition of HO-1 activity. We examined this hypothesis by altering cellular levels of HO-1 in human ovarian (A2780) and prostate cancer (DU145) cells and found that ZnPP inhibits cancer cell viability through an HO-1-independent mechanism. Neither over-expression nor knockdown of HO-1 significantly alters ZnPP's cytotoxicity in human cancer cells, indicating that HO-1 does not mediate ZnPP's inhibitory effect on cancer cell growth. Consistent with these observations, tin protoporphyrin (SnPP), a well-established HO-1 inhibitor, was found to be much less cytotoxic than ZnPP, and docosahexaenoic acid (DHA), an HO-1 inducer, enhanced ZnPP's cytotoxicity. In an effort to define the mechanisms of ZnPP-induced cytotoxicity, we found that ZnPP but not SnPP, diminished β-catenin expression through proteasome degradation and potently suppressed β-catenin-mediated signaling in our model systems. Thus, ZnPP-induced cytotoxicity is independent of HO-1 expression in cancer cells and the Wnt/β-catenin pathway is potentially involved in ZnPP's anticancer activity.

journal_name

Biochem Pharmacol

journal_title

Biochemical pharmacology

authors

Wang S,Avery JE,Hannafon BN,Lind SE,Ding WQ

doi

10.1016/j.bcp.2013.03.011

subject

Has Abstract

pub_date

2013-06-01 00:00:00

pages

1611-8

issue

11

eissn

0006-2952

issn

1873-2968

pii

S0006-2952(13)00192-5

journal_volume

85

pub_type

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