Distinctive traits of normal and tumor-derived human mammary epithelial cells expressed in a medium that supports long-term growth of both cell types.

Band, Vimla; Sager, Ruth

doi:10.1073/pnas.86.4.1249

Cited by 232 publications

(175 citation statements)

References 21 publications

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“…10,30 Therefore, we used retroviral infection to stably overexpress Ecd and/or H-RasQ61L in hTERT-immortalized but non-tumorigenic hMEC line 76N.TERT that is strictly dependent on exogenous growth factors for cell cycle progression and proliferation. 7,8 Western blot analysis of cell lysates confirmed the expression of overexpressed Ecd and/or Ras in respective single or double transductants ( Fig. 2A).…”

Section: Ecd Overexpression Synergizes With Mutant H-ras To Promote Cmentioning

confidence: 96%

“…8 The human Ecd cDNA sequence was cloned in the pMSCV-puro retroviral vector (Clonetech) to yield pMSCVpuro-Ecd. pBABE-hygro-H-RasQ61L (mutant Ras) was used to overexpress Ras.…”

Section: Methodsmentioning

confidence: 99%

“…For this purpose, cells were cultured for 72 hours in growth factor deprivation conditions (DFCI-3) and then supplemented with complete medium DFCI-1. 8 Prior to shifting the cultures into growth factor-containing medium p-AKT and p-ERK signals were relatively low and comparable between the control and various transductants (0 time points- Fig. 2B).…”

Section: Ecd Overexpression Synergizes With Mutant H-ras To Promote Cmentioning

confidence: 99%

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The cell cycle regulator ecdysoneless cooperates with H-Ras to promote oncogenic transformation of human mammary epithelial cells

et al. 2015

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Section: Ecd Overexpression Synergizes With Mutant H-ras To Promote Cmentioning

confidence: 96%

“…8 The human Ecd cDNA sequence was cloned in the pMSCV-puro retroviral vector (Clonetech) to yield pMSCVpuro-Ecd. pBABE-hygro-H-RasQ61L (mutant Ras) was used to overexpress Ras.…”

Section: Methodsmentioning

confidence: 99%

Section: Ecd Overexpression Synergizes With Mutant H-ras To Promote Cmentioning

confidence: 99%

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The cell cycle regulator ecdysoneless cooperates with H-Ras to promote oncogenic transformation of human mammary epithelial cells

et al. 2015

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“…HLE, HLF, HepG2, HepG2.2.15, and Alexander were maintained in RPMI (Gibco), supplemented with 10% (v/v) FCS, L-glutamine, penicillin, and streptomycin. MCF-10 cells were maintained in a DFCI-enriched medium as described (Band and Sager, 1989). All cells were maintained at 37°C in a humidified incubator containing 5% CO 2 .…”

Section: Cell Culturementioning

confidence: 99%

Human Hepatocellular Carcinoma (HCC) Cells Require Both α3β1 Integrin and Matrix Metalloproteinases Activity for Migration and Invasion

Giannelli

Bergamini

Fransvea

et al. 2001

Laboratory Investigation

133

134

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SUMMARY:Hepatocellular carcinoma (HCC) is the most frequent malignant tumor of the liver; prognosis depends on the tendency to metastasize. Cancer cell invasion is regulated by proteolytic remodeling of extracellular matrix components and by integrin expression. We have shown that matrix metalloproteinase-2 (MMP-2) and membrane-type-1 matrix metalloproteinase (MT1-MMP) cleave Laminin-5 (Ln-5), stimulating cell migration. Here we report that all HCC cells express MT1-MMP, migrate on Ln-1 and Collagen IV, whereas only HCC cells that express ␣3␤1 integrin secrete detectable levels of gelatinases, migrate on Ln-5, and invade through a reconstituted basement membrane (BM). Migration on Ln-5 is blocked by BB-94, an MMP inhibitor, and by MIG1, a monoclonal antibody that hinders migration on MMP-2-cleaved Ln-5. Invasion through a reconstituted BM is also inhibited by BB-94. HCC ␣3␤1-negative cells migrate on Ln-1 and Collagen IV, but not on Ln-5, and do not invade through a reconstituted BM, although they express MT1-MMP. Anti-␣3␤1 blocking antibodies inhibit gelatinase activation, cell motility, and cell invasion through Matrigel. In vivo, ␣3␤1 integrin and Ln-5 are expressed in HCC tissue but not in normal liver. In conclusion, our data suggest that both ␣3␤1 integrin and gelatinase activity are required for HCC migration and invasion. (Lab Invest 2001, 81:613-627).

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“…29 804G cells, derived from a rat urinary bladder carcinoma, were cultured in DMEM medium, supplemented with 10% fetal bovine serum, 2 mmol/L L-glutamine, penicillin (20 U/ml), and streptomycin (20 mg/ml).…”

Section: Cell Culturesmentioning

confidence: 99%

Expression of Matrix Metalloprotease-2-Cleaved Laminin-5 in Breast Remodeling Stimulated by Sex Steroids

Giannelli¹,

Pozzi²,

Stetler-Stevenson³

et al. 1999

The American Journal of Pathology

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The extracellular matrix plays an important role in breast remodeling. We have shown that matrix metalloprotease-2 (MMP2) cleaves laminin-5 (Ln-5), a basement membrane component , generating a fragment called ␥2x. Human breast epithelial cells , while constitutively immobile on intact Ln-5 , acquire a motile phenotype on MMP2-cleaved Ln-5. We hypothesize that this mechanism may underlie cell mobilization across the basement membrane during branching morphogenesis in breast development regulated by sex steroids. We report that the expression of MMP2 and cleavage of Ln-5 correlate well with tissue remodeling and epithelial rearrangement of the breast both in vivo and in vitro. Thus , the Ln-5 ␥2x fragment was detected by immunoblotting in sexually mature , pregnant , and postweaning , but not in prepubertal or lactating mammary glands. Furthermore, cleaved Ln-5 , as well as MMP2 , became detectable in remodeling glands from sexually immature rats treated with sex steroids. In rat mammary gland explants , epithelial reorganization and luminal cell morphological changes were induced by the addition of exogenous MMP2 , in parallel to the appearance of cleaved Ln-5. Similar effects were observed in epithelial monolayers plated on human Ln-5 and exposed to MMP2. These results suggest that cleavage of Ln-5 by MMP2 might be regulated by sex steroids and that it may contribute to breast remodeling under physiological and possibly pathological conditions. (Am J Pathol 1999, 154:1193-1201)

show abstract

Distinctive traits of normal and tumor-derived human mammary epithelial cells expressed in a medium that supports long-term growth of both cell types.

Cited by 232 publications

References 21 publications

The cell cycle regulator ecdysoneless cooperates with H-Ras to promote oncogenic transformation of human mammary epithelial cells

The cell cycle regulator ecdysoneless cooperates with H-Ras to promote oncogenic transformation of human mammary epithelial cells

Human Hepatocellular Carcinoma (HCC) Cells Require Both α3β1 Integrin and Matrix Metalloproteinases Activity for Migration and Invasion

Expression of Matrix Metalloprotease-2-Cleaved Laminin-5 in Breast Remodeling Stimulated by Sex Steroids

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