Role of Apoptosis in the Growth Inhibitory Effects of Vitamin D in MCF-7 Cells

1995 ◽  
pp. 45-52 ◽  
Author(s):  
JoEllen Welsh ◽  
Maura Simboli-Campbell ◽  
Carmen J. Narvaez ◽  
Martin Tenniswood
Keyword(s):  
Vitamin D ◽  
Inhibitory Effects ◽  
Growth Inhibitory ◽  
Mcf 7

Antiproliferative effects induced by guanine-based purines require hypoxanthine-guanine phosphoribosyltransferase activity

2010 ◽  
Vol 391 (9) ◽  
Author(s):  
Roberta Garozzo ◽  
Maria Angela Sortino ◽  
Carlo Vancheri ◽  
Daniele Filippo Condorelli
Keyword(s):  
Cell Line ◽  
Glioma Cell Line ◽  
Inhibitory Effects ◽  
Antiproliferative Effects ◽  
Growth Inhibitory ◽  
Tumoral Cell ◽  
A Cell ◽  
Hypoxanthine Guanine Phosphoribosyltransferase ◽  
U87 Cells

Abstract Guanine (GUA), guanosine and GMP exert a marked growth inhibition on the U87 glioma cell line that is not seen with other tested nucleotides, nucleosides and nucleobases. This effect could be replicated in several different human tumoral cell lines. Guanine shows a higher potency than guanosine or GMP, and co-treatments with adenosine or adenine are able to antagonize or revert the antiproliferative effect of guanine. The loss of the guanine effect in a cell line bearing a mutated inactive hypoxanthine-guanine phosphoribosyltransferase (HGPRT), and the decreased potency of GUA in U87 cells silenced for HGPRT transcripts, demonstrates the central role of the intracellular metabolism of GUA for growth-inhibitory effects. Considering the potential application of growth-inhibitory substances in anticancer therapy, knowledge of the molecular mechanism underlying GUA-induced effects encourages studies aimed at defining possible tumoral targets for experimental therapies.

Potentiation of the Growth-Inhibitory Effects of Vitamin D in Prostate Cancer by Genistein

2007 ◽  
Vol 65 (8) ◽  
pp. 121-123 ◽  
Author(s):  
Aruna V. Krishnan ◽  
Srilatha Swami ◽  
Jacqueline Moreno ◽  
Rumi B. Bhattacharyya ◽  
Donna M. Peehl ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Vitamin D ◽  
Inhibitory Effects ◽  
Growth Inhibitory

scholarly journals Growth-inhibitory effects of vitamin D analogues and retinoids on human pancreatic cancer cells

1996 ◽  
Vol 73 (11) ◽  
pp. 1341-1346 ◽  
Author(s):  
G Zugmaier ◽  
R Jäger ◽  
B Grage ◽  
MM Gottardis ◽  
K Havemann ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Vitamin D ◽  
Cancer Cells ◽  
Human Pancreatic Cancer ◽  
Inhibitory Effects ◽  
Pancreatic Cancer Cells ◽  
Vitamin D Analogues ◽  
Growth Inhibitory

Potentiation of the Growth-Inhibitory Effects of Vitamin D in Prostate Cancer by Genistein

2008 ◽  
Vol 65 ◽  
pp. S121-S123
Author(s):  
Aruna V. Krishnan ◽  
Srilatha Swami ◽  
Jacqueline Moreno ◽  
Rumi B. Bhattacharyya ◽  
Donna M. Peehl ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Vitamin D ◽  
Inhibitory Effects ◽  
Growth Inhibitory

Growth-inhibitory effects of the natural phyto-oestrogen genistein in MCF-7 human breast cancer cells

1994 ◽  
Vol 30 (11) ◽  
pp. 1675-1682 ◽  
Author(s):  
M.C. Pagliacci ◽  
M. Smacchia ◽  
G. Migliorati ◽  
F. Grignani ◽  
C. Riccardi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Inhibitory Effects ◽  
Growth Inhibitory ◽  
Mcf 7

Targeting of SMAD5 Links MicroRNA-155 to the TGFβ Pathway and Lymphomagenesis.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 315-315
Author(s):  
Deepak Rai ◽  
Sang-Woo Kim ◽  
Morgan R McKeller ◽  
Ricardo C Aguiar
Keyword(s):  
Cell Lines ◽  
B Cell Lymphoma ◽  
Type I ◽  
Inhibitory Effects ◽  
Tgfβ Receptors ◽  
Growth Inhibitory ◽  
The Impact ◽  
Tgfβ Pathway

Abstract Abstract 315 The mechanisms by which microRNA (miRNA) dysfunction contribute to the pathogenesis of diffuse large B-cell lymphoma (DLBCL) are not well established. MiRNAs are small non-protein coding RNAs that function by regulating the expression of target transcripts. Thus, to capture the physiologic and pathologic impact of these small regulatory molecules it is necessary to identify the genes that they inhibit. MicroRNA-155 (miR-155) is overexpressed in aggressive subsets of DLBCL, and its enforced expression in a transgenic, Eμ-miR-155, mouse model is associated with the development of lymphoblastic leukemia/high grade lymphoma. However, although a series of bona-fide miR-155 targets have been identified, it is still unclear how overexpression of this miR-155 contributes to lymphomagenesis. Starting from unbiased genome-wide approaches in DLBCL, we discovered that miR-155 directly binds to two sites in the 3'UTR of the SMAD5 gene, inhibiting its expression. Surprisingly, although SMAD5 activity is classically associated with signals transduced by bone morphogenic protein (BMP) family of cytokines, we found that in DLBCLs a non-canonical signaling module linking TGFβ1 to SMAD5 is also active. Furthermore, using kinase inhibitors specific to BMP or TGFβ receptors, we found that the type I TGFβ receptors, in particular ALK5, were essential for the activation of SMAD5 by TGFβ1 in DLBCL. These data suggested that the impact of miR-155 on the TGFβ pathway could be broader than previously appreciated, and abrogate the growth inhibitory effects of both BMP and TGFβ1 in DLBCL. To test this hypothesis, we generated DLBCL cell lines (Ly1, Ly18 and Ly19) ectopically expressing miR-155 and found that they became resistant to the cytostatic effects of TGFβ1 and BMPs. This blockade in growth inhibition was associated with an impaired cell cycle arrest and defective induction of p21. Next, to firmly establish the role of SMAD5 targeting in the miR-155-mediated disruption of the TGFβ signals, we created DLBCL cell lines stably expressing two independent SMAD5-shRNA constructs. Indeed, knockdown of SMAD5 in DLBCL limited the growth inhibitory effects of BMP and TGFβ1 and abrogated p21 induction, largely recapitulating the effects of miR-155 expression. In addition, using a xenograft model of DLBCL with in vivo luminescent imaging capabilities, we found that miR-155 overexpression yielded larger and more widespread lymphomas. Confirming our in vitro data, DLBCLs with stable SMAD5 knockdown were also more aggressive, indicating that SMAD5 downregulation phenocopies the effects of miR-155 in vivo. To gain further insights into the functional consequences of the miR-155/SMAD5 interplay, we used real-time RT-PCR to measure the transcriptional activation of several SMAD5 direct targets. In DLBCL cell lines ectopically expressing miR-155 or SMAD5 shRNA constructs, we found that the expression of the SMAD5 targets, ID1, ID2, SMAD6, SMAD7, BMPR2 and BMP6, was significantly diminished. These data further stressed the relevance of miR-155-mediated SMAD5 downregulation, and started to unveil the downstream components of SMAD5's tumor suppressive activities. Finally, we expanded our observations to primary tumors, and used western blotting to show that miR-155 overexpressing DLBCLs had significantly lower levels of SMAD5, and exhibited an impaired expression of its transcriptional targets. Together, our data instructed on miR-155 mediated lymphomagenesis, highlighted a hitherto unappreciated role of SMAD5 as a lymphoma suppressor gene, and defined a novel mechanism used by cancer cells to escape TGFβ growth inhibitory effects. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Mechanisms Mediating the Effects ofγ-Tocotrienol When Used in Combination with PPARγAgonists or Antagonists on MCF-7 and MDA-MB-231 Breast Cancer Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-17 ◽  
Author(s):  
Abhita Malaviya ◽  
Paul W. Sylvester
Keyword(s):  
Breast Cancer ◽  
Combined Treatment ◽  
Breast Cancer Cell Lines ◽  
Inhibitory Effects ◽  
Cancer Proliferation ◽  
Growth And Survival ◽  
Transcription Activity ◽  
Growth Inhibitory ◽  
Breast Cancer Growth ◽  
Mcf 7

γ-Tocotrienol is a natural vitamin E that displays potent anticancer activity, and previous studies suggest that these effects involve alterations in PPARγactivity. Treatment with 0.5–6 μM  γ-tocotrienol, 0.4–50 μM PPARγagonists (rosiglitazone or troglitazone), or 0.4–25 μM PPARγantagonists (GW9662 or T0070907) alone resulted in a dose-responsive inhibition of MCF-7 and MDA-MB-231 breast cancer proliferation. However, combined treatment of 1–4 μM  γ-tocotrienol with PPARγagonists reversed the growth inhibitory effects ofγ-tocotrienol, whereas combined treatment of 1–4 μM  γ-tocotrienol with PPARγantagonists synergistically inhibited MCF-7 and MDA-MB-231 cell growth. Combined treatment ofγ-tocotrienol and PPARγagonists caused an increase in transcription activity of PPARγalong with increased expression of PPARγand RXR, and decrease in PPARγcoactivators, CBP p/300, CBP C-20, and SRC-1, in both breast cancer cell lines. In contrast, combined treatment ofγ-tocotrienol with PPARγantagonists resulted in a decrease in transcription activity of PPARγ, along with decreased expression of PPARγand RXR, increase in PPARγcoactivators, and corresponding decrease in PI3K/Akt mitogenic signaling in these cells. These findings suggest that elevations in PPARγare correlated with increased breast cancer growth and survival, and treatment that decreases PPARγexpression may provide benefit in the treatment of breast cancer.

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