Control of skin cancer by the circadian rhythm

被引：185

作者：

Gaddameedhi, Shobhan ^{[1
,3
]}

Selby, Christopher P. ^{[1
]}

Kaufmann, William K. ^{[2
,3
,4
]}

Smart, Robert C. ^{[5
]}

Sancar, Aziz ^{[1
,3
,4
]}

机构：

[1] Univ N Carolina, Sch Med, Dept Biochem & Biophys, Chapel Hill, NC 27599 USA

[2] Univ N Carolina, Sch Med, Dept Pathol & Lab Med, Chapel Hill, NC 27599 USA

[3] Univ N Carolina, Sch Med, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA

[4] Univ N Carolina, Sch Med, Ctr Environm Hlth & Susceptibil, Chapel Hill, NC 27599 USA

[5] N Carolina State Univ, Dept Environm & Mol Toxicol, Cell Signaling & Canc Grp, Raleigh, NC 27695 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2011年 / 108卷 / 46期

基金：

美国国家卫生研究院;

关键词：

circadian clock; cryptochrome; sunbathing; tanning salons; NUCLEOTIDE EXCISION-REPAIR; XERODERMA-PIGMENTOSUM; HAIRLESS MOUSE; CLOCK GENES; C/EBP-ALPHA; DNA-DAMAGE; CELLS; UV; EXPRESSION; PROLIFERATION;

D O I：

10.1073/pnas.1115249108

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

070301 [无机化学]; 070403 [天体物理学]; 070507 [自然资源与国土空间规划学]; 090105 [作物生产系统与生态工程];

摘要：

Skin cancer is the most common form of cancer in the United States. The main cause of this cancer is DNA damage induced by the UV component of sunlight. In humans and mice, UV damage is removed by the nucleotide excision repair system. Here, we report that a rate-limiting subunit of excision repair, the xeroderma pigmentosum group A (XPA) protein, and the excision repair rate exhibit daily rhythmicity in mouse skin, with a minimum in the morning and a maximum in the afternoon/evening. In parallel with the rhythmicity of repair rate, we find that mice exposed to UV radiation (UVR) at 4:00 AM display a decreased latency and about a fivefold increased multiplicity of skin cancer (invasive squamous cell carcinoma) than mice exposed to UVR at 4:00 PM. We conclude that time of day of exposure to UVR is a contributing factor to its carcinogenicity in mice, and possibly in humans.

引用

页码：18790 / 18795

页数：6

共 37 条

[1]

Noninvasive method for assessing the human circadian clock using hair follicle cells [J].

Akashi, Makoto ;

Soma, Haruhiko ;

Yamamoto, Takuro ;

Tsugitomi, Asuka ;

Yamashita, Shiko ;

Yamamoto, Takuya ;

Nishida, Eisuke ;

Yasuda, Akio ;

Liao, James K. ;

Node, Koichi .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2010, 107 (35) :15643-15648

[2]

[Anonymous], 2008, Cancer facts and figures

[3]

Circadian Proteins and Genotoxic Stress Response [J].

Antoch, Marina P. ;

Kondratov, Roman V. .

CIRCULATION RESEARCH, 2010, 106 (01) :68-78

[4]

The hairless mouse in skin research [J].

Benavides, Fernando ;

Oberyszyn, Tatiana M. ;

VanBuskirk, Anne M. ;

Reeve, Vivienne E. ;

Kusewitt, Donna F. .

JOURNAL OF DERMATOLOGICAL SCIENCE, 2009, 53 (01) :10-18

[5]

Circadian expression of clock genes in human oral mucosa and skin : Association with specific cell-cycle phases [J].

Bjarnason, GA ;

Jordan, RCK ;

Wood, PA ;

Li, Q ;

Lincoln, DW ;

Sothern, RB ;

Hrushesky, WJM ;

Ben-David, Y .

AMERICAN JOURNAL OF PATHOLOGY, 2001, 158 (05) :1793-1801

[6]

Prevention of non-melanoma skin cancer by targeting ultraviolet-B-light signalling [J].

Bowden, GT .

NATURE REVIEWS CANCER, 2004, 4 (01) :23-35

[7]

A ROLE FOR SUNLIGHT IN SKIN-CANCER - UV-INDUCED P53 MUTATIONS IN SQUAMOUS-CELL CARCINOMA [J].

BRASH, DE ;

RUDOLPH, JA ;

SIMON, JA ;

LIN, A ;

MCKENNA, GJ ;

BADEN, HP ;

HALPERIN, AJ ;

PONTEN, J .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (22) :10124-10128

[8]

A REVIEW AND MATHEMATICAL-ANALYSIS OF CIRCADIAN-RHYTHMS IN CELL-PROLIFERATION IN MOUSE, RAT, AND HUMAN EPIDERMIS [J].

BROWN, WR .

JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1991, 97 (02) :273-280

[9]

DEFECTIVE REPAIR REPLICATION OF DNA IN XERODERMA PIGMENTOSUM [J].

CLEAVER, JE .

NATURE, 1968, 218 (5142) :652-&

[10]

XPA-deficiency in hairless mice causes a shift in skin tumor types and mutational target genes after exposure to low doses of UVB [J].

de Vries, A ;

Berg, RJW ;

Wijnhoven, S ;

Westerman, A ;

Wester, PW ;

van Kreijl, CF ;

Capel, PJA ;

de Gruijl, FR ;

van Kranen, HJ ;

van Steeg, H .

ONCOGENE, 1998, 16 (17) :2205-2212

← 1 2 3 4 →