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1.
Fig 3

Fig 3. From: PDX-1: Demonstration of Oncogenic Properties in Pancreatic Cancer.

HEK 293, MIA PaCa2 and HPDE cells stably overexpressing PDX-1 were cultured with and without human PDX-1 shRNA, then transferred into invasion inserts for 48h (Fig 3A). Increased quantatative invasiveness iss shown in 3B, 3C and 3D.

Shi-He Liu, et al. Cancer. ;117(4):723-733.
2.
Fig 1

Fig 1. From: PDX-1: Demonstration of Oncogenic Properties in Pancreatic Cancer.

Transient expression of PDX-1 increases cell proliferation. HEK 293, MIA PaCa2 and HPDE cells were transfected with human PDX-1 with and without human PDX-1 shRNA. Transient burst expression of PDX-1 results in increased cell proliferation in HEK 293 (A), MIA PACa2 (B) and HPDE (C) cells (P<0.05, respectively). PDX-1 shRNA co-transfection blocks the effect of cell proliferation (white bar).

Shi-He Liu, et al. Cancer. ;117(4):723-733.
3.
Fig 2

Fig 2. From: PDX-1: Demonstration of Oncogenic Properties in Pancreatic Cancer.

HEK 293, MIA PaCa2 and HPDE cells stably expressing PDX-1 with and without human PDX-1 shRNA had increased cell proliferation. PDX-1 overexpression caused significant increase of cell proliferation in all cell lines as shown in A, B and C. PDX-1 shRNA co-transfection was able to reverse the effect induced by PDX-1.

Shi-He Liu, et al. Cancer. ;117(4):723-733.
4.
Fig 4

Fig 4. From: PDX-1: Demonstration of Oncogenic Properties in Pancreatic Cancer.

PDX-1 overexpression in HEK 293 (A, G) and MIA PaCa2 (D, H) cells causes cell transformation in anchorage-independent growth assay. Colonies were photographed at 21 days under a phase contrast fluorescent microscope. The number and size of colonies were counted and calculated from each experiment at B, E and C, F, and the experiment was reproduced 5 times.

Shi-He Liu, et al. Cancer. ;117(4):723-733.
5.
Fig 6

Fig 6. From: PDX-1: Demonstration of Oncogenic Properties in Pancreatic Cancer.

PDX-1 regulates cell cycle proteins. Immunostaining study was performed on tumor sections using anti-PDX-1, P53 and PCNA antibodies. Red staining in upper panel and middle panel of A indicates PDX-1 and P53 expression, respectively, and green staining at bottom of panel A represented PCNA expression. Quantity was defined as positive cells in total cells as analyzed by image J and shown in B. Magnification×200.

Shi-He Liu, et al. Cancer. ;117(4):723-733.
6.
Fig 7

Fig 7. From: PDX-1: Demonstration of Oncogenic Properties in Pancreatic Cancer.

PDX-1 overexpression results in cell cycle disruption. Western blot was performed on PDX-1 stably trasnfected HEK 293 cells with or without PDX-1 shRNA. Protein levels of PDX-1, cyclin E, cdk2 P21, p27 and P53 were determined by bands profiles (A) and quantified by relative dentistry of aimed band vs internal control (B).

Shi-He Liu, et al. Cancer. ;117(4):723-733.
7.
Fig 5

Fig 5. From: PDX-1: Demonstration of Oncogenic Properties in Pancreatic Cancer.

PDX-1 overexpression promotes tumor formation and growth in SCID mice. HEK 293 or MIA PaCa2 cells overexpressing PDX-1 vs empty vector were implanted in SCID. Gross tumor volume at 30 days was was evaluated compared using x2 test (A) and tumor size was measured and compared using Student’s t test(B). Tumor size was significantly induced by PDX-1 overexpression in HEK 293 cells (A, B) and MIA PaCa2(C, D).

Shi-He Liu, et al. Cancer. ;117(4):723-733.
8.
Fig 8

Fig 8. From: PDX-1: Demonstration of Oncogenic Properties in Pancreatic Cancer.

PDX-1 knockdown of PANC-1 cells with high endogenous PDX-1 expression affected gene expression in signaling pathways of cell proliferation, invasion, apoptosis and angiogenesis using Affymetrix GeneChip arrays (Human Genome U133 Plus 2.0 Array). Molecules in red represent gene over-expression, whereas molecules in green represent down regulation. Direct interactions are indicated as (green) promoting or (red) inhibiting interacting arrows. PDX-1 knockdown stimulates apoptosis and cell cycle arrest by downregulation of cyclins. Decreased gene expression related to angiogenesis (VEGF) and invasion (HBEGF, PAI-1, uPA) was also seen in the analysis.

Shi-He Liu, et al. Cancer. ;117(4):723-733.

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