Transcriptional regulation of laminin gene expression

Aberdam, Daniel; Virolle, Thierry; Simon‐Assmann, Patricia

doi:10.1002/1097-0029(20001101)51:3<228::aid-jemt3>3.0.co;2-9

Cited by 26 publications

(12 citation statements)

References 72 publications

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“…The Lama1 gene, like other laminin genes (9,44,45), is a TATA box-less gene. The combined study of progressive deletions and of individual site mutations of the 2-kb promoter pointed to the major role of an Sp1-binding element (located at position Ϫ73 bp from the translation start site) in the basal transcriptional activity.…”

Section: Discussionmentioning

confidence: 99%

Krüppel-like Factors Regulate the Lama1 Gene Encoding the Laminin α1 Chain

Piccinni¹,

Bolcato-Bellemin²,

Klein³

et al. 2004

Journal of Biological Chemistry

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Laminin-1 (␣1␤1␥1), a basement membrane (BM) constituent, has been associated with differentiation processes and also with malignant progression. In the intestinal tissue, the ␣1 chain is expressed and secreted in the subepithelial BM during the developmental period; in the adult rodent tissue, it is restricted to the BM of the dividing cells. To understand how laminin ␣1 chain expression is regulated, we cloned and characterized a 2-kb promoter region of the Lama1 mouse gene. Analysis of the promoter was conducted in the Caco2-TC7 intestinal epithelial cells by transient transfection of serially deleted and site-directed mutated promoter constructs, by electrophoretic mobility shift assays, and expression of selected transcription factors. We determined that a proximal region, which includes an Sp1-binding GC box and a Krü ppel-like element, was important for the promoter activity. This region is conserved between the human and mouse genes. Interestingly, two Krü ppellike factors KLF4 and KLF5 exhibit opposing effects on the Lama1 promoter activity that are decreased and increased, respectively, in the intestinal epithelial cells. These data corroborate the complementary expression of KLF4 and KLF5 along the intestinal crypt-villus axis and the parallel expression of KLF5 and laminin ␣1 chain in the crypt region. Finally, we showed that glucocorticoids stimulate the promoter activity. This study is the first characterization of the Lama1 promoter; we identified regulatory elements that may account for the expression pattern of the endogenous protein in the mouse intestine.

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Section: Discussionmentioning

confidence: 99%

Krüppel-like Factors Regulate the Lama1 Gene Encoding the Laminin α1 Chain

Piccinni¹,

Bolcato-Bellemin²,

Klein³

et al. 2004

Journal of Biological Chemistry

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“…Laminins are ECM glycoproteins that promote mammary gland homeostasis by regulating cell adhesion, migration, proliferation, differentiation and angiogenesis (Aberdam et al, 2000). Laminins have three distinct protein subunits, designated ␣, ␤ and ␥.…”

Section: Introductionmentioning

confidence: 99%

CREB-binding protein regulates apoptosis and growth of HMECs grown in reconstituted ECM via laminin-5

Dietze

Bowie

Mrózek

et al. 2005

Journal of Cell Science

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Interactions between normal mammary epithelial cells and extracellular matrix (ECM) are important for mammary gland homeostasis. Loss of interactions between ECM and normal mammary epithelial cells are thought to be an early event in mammary carcinogenesis. CREB-binding protein (CBP) is an important regulator of proliferation and apoptosis but the role of CBP in ECM signaling is poorly characterized. CBP was suppressed in basal-cytokeratin-positive HMECs (CK5/6+, CK14+, CK8–, CK18–, CK19–). Suppression of CBP resulted in loss of reconstituted ECM-mediated growth control and apoptosis and loss of laminin-5 α3-chain expression. Suppression of CBP in normal human mammary epithelial cells (HMECs) resulted in loss of CBP occupancy of the LAMA3A promoter and decreased LAMA3A promoter activity and laminin-5 α-3 chain expression. Exogenous expression of CBP in CBP-negative HMECs that have lost reconstituted ECM-mediated growth regulation and apoptosis resulted in (1) CBP occupancy of the LAMA3A promoter, (2) increased LAMA3A activity and laminin-5 α3-chain expression, and (3) enhancement of reconstituted ECM-mediated growth regulation and apoptosis. Similarly, suppression of laminin-5 α3-chain expression in HMECs resulted in loss of reconstituted ECM-mediated growth control and apoptosis. These observations suggest that loss of CBP in basal-cytokeratin-positive HMECs results in loss of reconstituted ECM-mediated growth control and apoptosis through loss of LAMA3A activity and laminin-5 α3-chain expression. Results in these studies may provide insight into early events in basal-type mammary carcinogenesis.

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“…Laminins are ECM glycoproteins that promote mammary gland homeostasis through regulating cell adhesion, migration, proliferation, differentiation, and angiogenesis (Aberdam et al, 2000). Laminins have three distinct protein subunits, designated a, p, and y.…”

Section: Referencesmentioning

confidence: 99%

CBP and Extracellular Matrix-Induced Apoptosis in p53(-) HMECs: A Model of Early Mammary Carcinogenesis

Seewaldt¹

2003

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Transcriptional regulation of laminin gene expression

Cited by 26 publications

References 72 publications

Krüppel-like Factors Regulate the Lama1 Gene Encoding the Laminin α1 Chain

Krüppel-like Factors Regulate the Lama1 Gene Encoding the Laminin α1 Chain

CREB-binding protein regulates apoptosis and growth of HMECs grown in reconstituted ECM via laminin-5

CBP and Extracellular Matrix-Induced Apoptosis in p53(-) HMECs: A Model of Early Mammary Carcinogenesis

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