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1.
Figure 3

Figure 3. KSHV induces intrinsic invasiveness for oral fibroblasts following de novo infection. From: Kaposi sarcoma-associated herpesvirus (KSHV) induces a functional tumor-associated phenotype for oral fibroblasts.

HGF and PDLF were incubated with purified KSHV as above, then relative invasiveness quantified 24 h later using matrigel-based transwell invasion assays as described in Methods. Error bars represent the S.E.M. for three independent experiments. **=p<0.01.

Lu Dai, et al. Cancer Lett. ;318(2):214-220.
2.
Figure 2

Figure 2. KSHV increases cytokine/chemokine secretion by oral fibroblasts following de novo infection. From: Kaposi sarcoma-associated herpesvirus (KSHV) induces a functional tumor-associated phenotype for oral fibroblasts.

HGF and PDLF were incubated with either virus-free media (mock) or purified KSHV for 2 h, followed by fresh media for an additional 24 h. Secreted factors were quantified within culture supernatants using commercial ELISA kits as described in Methods. Error bars represent the S.E.M. for three independent experiments. **=p<0.01.

Lu Dai, et al. Cancer Lett. ;318(2):214-220.
3.
Figure 7

Figure 7. LANA induces emmprin expression and cell invasiveness for oral fibroblasts. From: Kaposi sarcoma-associated herpesvirus (KSHV) induces a functional tumor-associated phenotype for oral fibroblasts.

(A) HGF were transfected with either control (pcDNA) or LANA-encoding (pcDNA-LANA) vectors for 48 h. LANA and emmprin expression were subsequently confirmed using immunoblots. (B) HGF were transfected as in (A) in the presence of either control non-target (n-siRNA) or emmprin-specific siRNA (e-siRNA), and invasion assessed as previously described. Error bars represent the S.E.M. for three independent experiments. ** = p < 0.01 for comparison of invasiveness for e-siRNA/pcDNA-LANA and n-siRNA/pcDNA-LANA cotransfectants.

Lu Dai, et al. Cancer Lett. ;318(2):214-220.
4.
Figure 5

Figure 5. KSHV induces VEGF secretion by oral fibroblasts through Sp1- and Egr2-mediated activation of emmprin. From: Kaposi sarcoma-associated herpesvirus (KSHV) induces a functional tumor-associated phenotype for oral fibroblasts.

HGF were transfected with either control non-target (n-siRNA), emmprin-siRNA (em-siRNA), Sp1-siRNA, or Egr2-siRNA for 48 h prior to their incubation with KSHV, then VEGF (A) and IL-8 (B) secretion were quantified within culture supernatants using ELISAs. In some groups, transfected cells were transduced with a recombinant adenoviral vector encoding emmprin (AdV-em) or a control vector (AdV) for 48 h prior to virus incubation. ** = p < 0.01 relative to n-siRNA+K group. ## = p < 0.01 relative to Sp1-siRNA+AdV+K or Egr2-siRNA+AdV+K groups. Error bars represent the S.E.M. for three independent experiments.

Lu Dai, et al. Cancer Lett. ;318(2):214-220.
5.
Figure 4

Figure 4. KSHV induces Sp1- and Egr2-dependent transcriptional activation of emmprin. From: Kaposi sarcoma-associated herpesvirus (KSHV) induces a functional tumor-associated phenotype for oral fibroblasts.

(A–B) HGF (A) and PDLF (B) were incubated with purified KSHV as described previously, then immunoblots were performed 24 h later to identify expression of high MW (~65 kDa) and low MW (~35 kDa) glycoforms of emmprin, as well as emmprin-associated MMPs. β-Actin was also identified for loading controls. (C–D) HGF were transfected with either control non-target (n-siRNA), emmprin-siRNA (em-siRNA), Sp1-siRNA or Egr2-siRNA for 48 h prior to their incubation with KSHV. 24 h later, protein (C) and transcript (D) expression were determined by immunoblots and qRT-PCR, respectively.

Lu Dai, et al. Cancer Lett. ;318(2):214-220.
6.
Figure 6

Figure 6. KSHV induces VEGF-mediated invasiveness for oral fibroblasts through activation of emmprin. From: Kaposi sarcoma-associated herpesvirus (KSHV) induces a functional tumor-associated phenotype for oral fibroblasts.

HGF were transfected with either control non-target (n-siRNA), emmprin-siRNA (em-siRNA), Sp1-siRNA, or Egr2-siRNA for 48 h prior to their incubation with either virus-free media (mock) or purified KSHV, then cell invasiveness quantified 24 h later using transwell invasion assays as described previously. In some groups, transfected cells were transduced with a recombinant adenoviral vector encoding emmprin (AdV-em) or a control vector (AdV) for 48 h prior to virus incubation. For some groups, 5 ng/mL recombinant human VEGF was added to the top of chambers. Error bars represent the S.E.M. for three independent experiments. ** = p < 0.01.

Lu Dai, et al. Cancer Lett. ;318(2):214-220.
7.
Figure 1

Figure 1. Establishment of latent KSHV infection within primary oral fibroblasts. From: Kaposi sarcoma-associated herpesvirus (KSHV) induces a functional tumor-associated phenotype for oral fibroblasts.

(A) HGF and PDLF were incubated with purified KSHV (MOI~10), or UV-inactivated KSHV as a negative control, for 2 h. After cells were incubated for an additional 24 h in fresh media, IFA were performed as in Methods to quantify expression of KSHV-encoded LANA as indicated by the typical intranuclear, punctate staining pattern (red dots). Nuclei were identified using DAPI (blue). (B–C) HGF (B) and PDLF (C) were incubated with KSHV as in (A). After 72 h, qRT-PCR was used to quantify expression of transcripts encoding latent (LANA, vFLIP, and vCyclin) and lytic (RTA, vGPCR, K8.1, and vIL-6) viral proteins as detailed in Methods. Error bars represent the S.E.M. for three independent experiments.

Lu Dai, et al. Cancer Lett. ;318(2):214-220.

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