Flow chart for the literature search in the meta-analysis.

<p>Flow chart for the literature search in the meta-analysis.</p

Associations between VDR polymorphisms (ApaI, BsmI, Cdx-2, FokI, TaqI) and the risk of ovarian cancer under different genetic models.

<p>Associations between VDR polymorphisms (ApaI, BsmI, Cdx-2, FokI, TaqI) and the risk of ovarian cancer under different genetic models.</p

LFG-500 inhibits the nuclear translocation of NF-κB rather than AP-1 or STAT3 in MDA-MB-231 cells.

<p>(<b>A</b>) LFG-500 has no significant effects on AP-1 or STAT3. Cells were treated with various concentrations (2, 4, and 8 μM) of LFG-500 for 24 h. The nuclear levels of the proteins were detected by Western blot assay using specific antibodies. Lamin-A was used as nuclear loading control. (<b>B</b>) LFG-500 inhibits the nuclear translocation of NF-κB. Cytosolic and nuclear extracts in the cells were prepared according to the “Materials and methods”. The nuclear and cytoplasmic levels of NF-κB p65 were determined by Western blot assay. (<b>C</b>) The inhibitory effect of LFG-500 on the nuclear translocation of NF-κB. MDA-MB-231 cells were immunostained with anti-NF-κB p65 (1∶50) and DAPI (×400, the scale bar represents 30 μm). (<b>D</b>) The effects of LFG-500 on phosphorylation levels of IKKα/β and IκBα. Cells were treated with various concentrations (2, 4, and 8 μM) of LFG-500 for 24 h, and the expression of target proteins was detected by Western blotting using specific antibodies where β-actin was used as loading control. <i>*P</i><0.05 or <i>**P</i><0.01 represents significant difference from the control group.</p

PI3K/AKT signaling pathway is involved in the inhibitory effect of LFG-500 on NF-κB activation.

<p>(<b>A</b>) LFG-500 has no influence on MAPK signaling pathway. MDA-MB-231 cells were treated with various concentrations (2, 4, and 8 μM) of LFG-500 for 24 h. Total expression and phosphorylation of ERK, JNK, and p38 were analyzed by Western blotting. β-actin was used as a loading control. (<b>B</b>) LFG-500 inhibits the expression of PI3K p85α/γ and p-AKT. The expression of target proteins was determined by Western blotting. Densitometric analysis of the proteins studied (right). <i>*P</i><0.05 or <i>**P</i><0.01 represents significant difference from the control group.</p

Forest plot for the association between variant FokI in the VDR and risk of ovarian cancer (TT vs. CC).

<p>NECC, new England case-control study; NHS, nurses’ health study; WHS, women’s health study; MALOVA, malignant ovarian cancer study; SEARCH, studies of epidemiology and risk factors in cancer heredity: ovarian cancer study; GEOCS, genetic epidemiology of ovarian cancer study; UKOPS, united kingdom ovarian cancer population study.</p

Characteristics of publications identified for the meta-analysis.

<p><b>Abbreviations:</b> PB, population-based case-control study; NCC, nested case-control study; PCR-RFLP, polymerase chain reaction-restriction fragment length polymorphism; NECC, new England case-control study; NHS, nurses’ health study; WHS, women’s health study; MALOVA, malignant ovarian cancer study; SEARCH, studies of epidemiology and risk factors in cancer heredity: ovarian cancer study; GEOCS, genetic epidemiology of ovarian cancer study; HAW, Hawaii ovarian cancer study; UKOPS, united kingdom ovarian cancer population study.</p

LFG-500 inhibits adhesion, migration, and invasion of MDA-MB-231 cells <i>in vitro</i>.

<p>(<b>A</b>) Chemical structure of LFG-500. (<b>B</b>) Inhibitory effect of LFG-500 on the growth of MDA-MB-231 cells for 24 h. MTT assay was employed. (<b>C</b>) Trypan blue dye exclusion assay of LFG-500 on the growth of MDA-MB-231 cells. Cells were treated with indicated concentrations of LFG-500 for 24 h. (<b>D</b>) LFG-500 (8 μM) has no influence on the normal size and shape of cells (×200, the scale bar represents 30 μm). (<b>E</b>) Inhibitory effect of LFG-500 on adhesion of MDA-MB-231 cells to fibronectin. Cell suspension (100 μl, 2×10⁵ cells/ml) was added to fibronectin pre-coated plates and incubated at 37°C for 1 h. Then culture media was carefully suctioned out. Each well was washed three times with PBS. MTT assay was adopted to determine the number of adherent cells. (<b>F</b>) LFG-500 inhibits cell migration. Cell monolayer was wounded by a 200 μL yellow pipette tip followed by treatment with various concentrations (2, 4, and 8 μM) of LFG-500 for 24 h. The number of the cells in the denuded zone was quantified under an inverted microscope. White lines indicate the wound edge. The migrated cells across the white lines were counted in six random fields from each treatment. Photographs of the wound of cells treated with LFG-500, ×100 (left). Quantification of the migrated cells (right). (<b>G</b>) LFG-500 inhibits cell invasion. Photographs of the invaded cell stained by hematoxylin and eosin, ×200 (left). Quantification of the invaded cells (right). <i>*P</i><0.05 or <i>**P</i><0.01 represents significant difference from the control group.</p

Forest plot for the association between variant FokI in the VDR and risk of ovarian cancer (CT vs. CC).

<p>NECC, new England case-control study; NHS, nurses’ health study; WHS, women’s health study; MALOVA, malignant ovarian cancer study; SEARCH, studies of epidemiology and risk factors in cancer heredity: ovarian cancer study; GEOCS, genetic epidemiology of ovarian cancer study; UKOPS, united kingdom ovarian cancer population study.</p

A possible mechanism underlying the inhibitory effect of LFG-500 on the invasion of cancer cells.

<p>A possible mechanism underlying the inhibitory effect of LFG-500 on the invasion of cancer cells.</p

Liposomal C8 ceramide administration inhibits HepG2 cell growth in SCID mice, while dramatically improving mice survival.

<p>HepG2 xenograft-bearing SCID mice (10 mice per group) were intravenously (<i>i</i>.<i>v</i>.) injected with liposomal C8 (5/15 mg/kg body weight, once every two days, 30 days), liposomal vehicle control (no ceramide, “Lipo Ctrl”) or Saline, HepG2 xenograft volumes (A) and mice body weights (D) were recorded every 10 days, tumor growth (in mm³/day) was also presented (B). Mice survival at day 50 was shown (C). At day 50, xenografted tumors were isolated (n = 3 for each group), expression of listed proteins in the tumor tissues was tested by Western blot (E-G). Protein expression was quantified (E-G). <i>In vivo</i> experiments were repeated twice, and similar results were obtained. * indicates statistically significant differences compared to “Saline” group.</p