Parathyroid hormone and the regulation of cell cycle in colon adenocarcinoma cells

被引：9

作者：

Calvo, Natalia ^{[1
]}

Gentili, Claudia ^{[1
]}

Russo de Boland, Ana ^{[1
]}

机构：

[1] Univ Nacl Sur, Dept Biol Bioquim & Farm, RA-8000 Bahia Blanca, Buenos Aires, Argentina

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 2011年 / 1813卷 / 10期

关键词：

PTH; Caco-2; cells; Cell cycle; PKC; DEPENDENT KINASE INHIBITOR; N-TERMINAL-KINASE; PROGNOSTIC-SIGNIFICANCE; SIGNAL-TRANSDUCTION; DOWN-REGULATION; PKC-ALPHA; ACTIVATION; CANCER; PTH; P27(KIP1);

D O I：

10.1016/j.bbamcr.2011.06.001

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Parathyroid hormone (PTH) functions as a major mediator of bone remodeling and as an essential regulator of calcium homeostasis. In this study, we investigated the role of PTH in the regulation of the cell cycle in human colon adenocarcinoma Caco-2 cells. Flow cytometry analysis revealed that PTH (10(-8) M, 12-24 h) treatment increases the number of cells in the G0/G1 phase and diminishes the number in both phases S and G2/M. In addition, analysis by Western blot showed that the hormone increases the expression of the inhibitory protein p27Kip1 and diminishes the expression of cyclin D1, cyclin D3 and CDK6. However, the amounts of CDK4, p21Cip1, p15INK4B and p16INK4A were not different in the absence or presence of PTH. Inhibitors of PKC (Ro-318220, bisindolylmaleimide and chelerythine), but not JNK (SP600125) and PP2A (okadaic acid and calyculin A), reversed PTH response in Caco-2 cells. Taken together, our results suggest that PTH induces G0/G1 phase arrest of Caco-2 intestinal cells and changes the expression of proteins involved in cell cycle regulation via the PKC signaling pathway. (C) 2011 Elsevier B.V. All rights reserved.

引用

页码：1749 / 1757

页数：9

共 55 条

[11] Serine/threonine protein kinases and apoptosis [J].

Cross, TG ;

Scheel-Toellner, D ;

Henriquez, NV ;

Deacon, E ;

Salmon, M ;

Lord, JM .

EXPERIMENTAL CELL RESEARCH, 2000, 256 (01) :34-41

[12] Cyclin D1 as a target for the proliferative effects of PTH and PTHrP in early osteoblastic cells [J].

Datta, Nabanita S. ;

Pettway, Glenda J. ;

Chen, Chen ;

Koh, Amy J. ;

McCauley, Laurie K. .

JOURNAL OF BONE AND MINERAL RESEARCH, 2007, 22 (07) :951-964

[13]

DEVAULT A, 1991, COLD SPRING HARB SYM, V56, P503

[14] PTH STIMULATES THE PROLIFERATION OF TE-85 HUMAN OSTEOSARCOMA CELLS BY A MECHANISM NOT INVOLVING EITHER INCREASED CAMP OR INCREASED SECRETION OF IGF-I, IGF-II OR TGF-BETA [J].

FINKELMAN, RD ;

MOHAN, S ;

LINKHART, TA ;

ABRAHAM, SM ;

BOUSSY, JP ;

BAYLINK, DJ .

BONE AND MINERAL, 1992, 16 (02) :89-100

[15]

Fishman DD, 1998, INT J ONCOL, V12, P181

[16] Protein kinase C signaling mediates a program of cell cycle withdrawal in the intestinal epithelium [J].

Frey, MR ;

Clark, JA ;

Leontieva, O ;

Uronis, JM ;

Black, AR ;

Black, JD .

JOURNAL OF CELL BIOLOGY, 2000, 151 (04) :763-777

[17] STRUCTURE-FUNCTION RELATIONSHIP OF PARATHYROID-HORMONE - ACTIVATION OF PHOSPHOLIPASE-C, PROTEIN KINASE-A AND KINASE-C IN OSTEOSARCOMA CELLS [J].

FUJIMORI, A ;

CHENG, SL ;

AVIOLI, LV ;

CIVITELLI, R .

ENDOCRINOLOGY, 1992, 130 (01) :29-36

[18]

Garrido-Gracia JC, 2006, J PHYSIOL BIOCHEM, V62, P35, DOI 10.1007/BF03165804

[19] Parathyroid hormone and parathyroid hormone-related peptide, and their receptors [J].

Gensure, RC ;

Gardella, TJ ;

Jüppner, H .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2005, 328 (03) :666-678

[20] Characterization of PTH/PTHrP receptor in rat duodenum: Effects of ageing [J].

Gentili, C ;

Morelli, S ;

de Boland, AR .

JOURNAL OF CELLULAR BIOCHEMISTRY, 2003, 88 (06) :1157-1167

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