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Antiapoptotic action of 1,25-dihydroxyvitamin D3 is associated with increased mitochondrial MCL-1 and RAF-1 proteins and reduced release of cytochrome c.

Abstract：

:Release of mitochondrial cytochrome c has been recently linked to the activation of the "executioner" phase of the cellular programs for death by apoptosis. This release is known to be negatively regulated by Bcl-2 and Bcl-XL proteins. We show here that treatment of human leukemia cells HL60 with 1,25-dihydroxyvitamin D3 (1,25D3) results in progressive increases in the levels of cellular antiapoptotic protein Mcl-1, a transient increase in Al protein level, but no increases in Bcl-2 or Bcl-XL proteins. The increase in Mcl-1 protein levels correlates with a reduced extent of apoptotic cell death induced by etoposide or the calcium ionophore A23187. The Mcl-1 protein is primarily localized in the mitochondria, and etoposide- or A23187-induced cytochrome c release is reduced in cells in which the mitochondria contain the Mcl-1 protein demonstrable by immunoblots. Raf-1 protein can also be detected in the mitochondrial fractions that contain Mcl-1 protein but not in the Mcl-1-negative fractions. These findings suggest that in these promyelocytic leukemia cells Mcl-1 has a function analogous to that of Bcl-2 in other cells, i.e., to target Raf-1 to mitochondria and to reduce cell damage-induced release of mitochondrial cytochrome c. Our findings provide a potential mechanism for the antiapoptotic action of 1,25D3 and show that differentiation and apoptosis signaling pathways not only interact but involve a proliferation-associated gene, Raf-1.

journal_name

Exp Cell Res

journal_title

Experimental cell research

authors

Wang X,Studzinski GP

doi

10.1006/excr.1997.3667

subject

Has Abstract

pub_date

1997-08-25 00:00:00

pages

210-7

issue

1

eissn

0014-4827

issn

1090-2422

pii

S0014-4827(97)93667-3

journal_volume

235

pub_type

杂志文章

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