Circadian regulation of cell cycle and apoptosis proteins in mouse bone marrow and tumor.

Circadian regulation of cell cycle and apoptosis proteins in mouse bone marrow and tumor. Research Abstract Details 

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Circadian regulation of cell cycle and apoptosis proteins in mouse bone marrow and tumor. Abstract Text:

Teresa G Granda,Xu-Hui Liu,Rune Smaaland,Nicolas Cermakian,Elisabeth Filipski,Paolo Sassone-Corsi,Francis ,

Proapoptotic drugs such as docetaxel displayed least toxicity and highest antitumor efficacy following dosing during the circadian rest phase in mice, suggesting that cell cycle and apoptotic processes could be regulated by the circadian clock. In study 1, mouse bone marrow and/or tumor were obtained every 4 h for 24 h in C3H/HeN mice with or without MA13/C mammary adenocarcinoma in order to determine the circadian patterns in cell-cycle phase distribution and BCL-2 anti-apoptotic protein expression. In study 2, mouse bone marrow from B6D2F1 mice was sampled every 3 h for 24 h in order to confirm the BCL-2 rhythm and to study its relation with 24 h changes in the expression of proapoptotic BCL-2-associated X protein (BAX) protein and clock genes mPer2, mBmal1, mClock, and mTim mRNAs. The rhythms in G1-, S- or G2/M-phase cells were shifted in tumor compared with bone marrow. In the tumor, the mean proportion of G2/M-phase cells increased by 75% from late rest to late activity span (P from cosinor = 0.001). No 24 h rhythm was found for BCL-2 in tumors. In contrast to this, in the bone marrow, mean BCL-2 expression varied 2.8-fold in B6D2F1 mice (P=0.025) and 3- or 4.5-fold in tumor-bearing and nontumor-bearing C3H/HeN mice, with a peak during the early rest span (P=0.024 and P<0.001, respectively). BAX varied fivefold during the 24 h span with a major peak occurring near mid-activity (P=0.007). The mean mRNAs of mPer2, mClock, and mBmal1 varied twofold to threefold over the 24 h, with high values during the activity span (P<0.05). In the tumor, the circadian organization in cell-cycle phase distribution was shifted and BCL2 rhythm was ablated. Conversely, a molecular circadian clock likely regulated BCL-2 and BAX expression in the bone marrow, increasing cellular protection against apoptosis during the rest span.

Circadian regulation of cell cycle and apoptosis proteins in mouse bone marrow and tumor. Publishing Authors By Initials

TG Granda,XH Liu,R Smaaland,N Cermakian,E Filipski,P Sassone-Corsi,F ,

For similar peptides: intracellular signaling peptides and proteins: apoptosis regulatory proteins: proto-oncogene proteins c-bcl-2: bcl-2-associated x protein research abstracts see: peptides: intracellular signaling peptides and proteins: apoptosis regulatory proteins: proto-oncogene proteins c-bcl-2: bcl-2-associated x protein research

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Circadian regulation of cell cycle and apoptosis proteins in mouse bone marrow and tumor. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The FASEB journal : official publication of the Fe

VOLUME: 19

Page Numbers: 304-6

Journal Abbreviation: FASEB J.

ISSN: 1530-6860

DAY: 15

MONTH: 11

YEAR: 2004

Circadian regulation of cell cycle and apoptosis proteins in mouse bone marrow and tumor. Information

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LANGUAGE: eng

NlmUniqueID: 8804484

Circadian regulation of cell cycle and apoptosis proteins in mouse bone marrow and tumor. Keywords Mesh Terms:

KEYWORDS: bcl-2-Associated X Protein

MESH TERMS: genetics

Chemical & Substance for Abstract: Circadian regulation of cell cycle and apoptosis proteins in mouse bone marrow and tumor. Information

Substance Name: docetaxel

Registry Number: 114977-28-5

Grant and Affiliation Information for Circadian regulation of cell cycle and apoptosis proteins in mouse bone marrow and tumor.

AFFILIATION: Cancer Chronotherapeutics, INSERM E 0354 and Université Paris XI, Hôpital Paul Brousse, Villejuif, France.

Country: United States

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MEDLINETA: FASEB J

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