Presentation is loading. Please wait.

Presentation is loading. Please wait.

CAFs enhance the acinar forming capacity of SOX2oe TUM622 cells and suppress dysplasia. CAFs enhance the acinar forming capacity of SOX2oe TUM622 cells.

Published byGlenna Irawan Modified over 6 years ago

Similar presentations

Presentation on theme: "CAFs enhance the acinar forming capacity of SOX2oe TUM622 cells and suppress dysplasia. CAFs enhance the acinar forming capacity of SOX2oe TUM622 cells."— Presentation transcript:

1 CAFs enhance the acinar forming capacity of SOX2oe TUM622 cells and suppress dysplasia.
CAFs enhance the acinar forming capacity of SOX2oe TUM622 cells and suppress dysplasia. (A) Quantification of spheroids formed from Vector and SOX2oe cells as monoculture/coculture with CAFs. Each column represents triplicates. Error bars represent SD. (B) CAFs induce the formation of acinar-like structures when in coculture with SOX2oe cells. Both Vector and SOX2oe spheroids become invasive when they are in close proximity with CAFs. (Scales bars, 100 μm.) (C) Immunofluorescence of SOX2oe monoculture as well as CAF cocultures stained for Vimentin (cytoplasmic)/p63 (nuclear), E-Cadherin, and ITGA6. Anti-vimentin and anti-p63 antibodies were stained with the same secondary antibody (green). (D) Immunofluorescence of SOX2oe monoculture as well as CAF cocultures stained for Vimentin, SOX2, and Phalloidin. (Scale bars, 50 μm.)‏ Shuang Chen et al. PNAS doi: /pnas ©2018 by National Academy of Sciences

Download ppt "CAFs enhance the acinar forming capacity of SOX2oe TUM622 cells and suppress dysplasia. CAFs enhance the acinar forming capacity of SOX2oe TUM622 cells."

Similar presentations

Supplementary Figure 2: PBX1 induces morphological and cytoskeletal changes consistent with differentiation in NB. A) Morphology of SHSY5Y cells. Cells.

Supplementary Figure 2: PBX1 induces morphological and cytoskeletal changes consistent with differentiation in NB. A) Morphology of SHSY5Y cells. Cells.
ORL1 inhibits axon regeneration.

ORL1 inhibits axon regeneration.
Type VIIa1 collagen and laminin-γ2 promote a p53 mutant/HIF-1–dependent proinvasive phenotype. Type VIIa1 collagen and laminin-γ2 promote a p53 mutant/HIF-1–dependent.

Type VIIa1 collagen and laminin-γ2 promote a p53 mutant/HIF-1–dependent proinvasive phenotype. Type VIIa1 collagen and laminin-γ2 promote a p53 mutant/HIF-1–dependent.
Chronic stress accelerated DSS-induced colitis.

Chronic stress accelerated DSS-induced colitis.
Identification and characterization of a xap5 mutant in Chlamydomonas.

Identification and characterization of a xap5 mutant in Chlamydomonas.
Loss of USP8 or HIF1α impairs endocytic recycling required for ciliogenesis Kinetic analysis of transferrin recycling measured by flow cytometry. Loss.

Loss of USP8 or HIF1α impairs endocytic recycling required for ciliogenesis Kinetic analysis of transferrin recycling measured by flow cytometry. Loss.
Transient overexpression of FveCYP707A4a delayed fruit ripening.

Transient overexpression of FveCYP707A4a delayed fruit ripening.
Expression of α5β1-integrin enhances EboV GP-mediated infection of GD25 cells. Expression of α5β1-integrin enhances EboV GP-mediated infection of GD25.

Expression of α5β1-integrin enhances EboV GP-mediated infection of GD25 cells. Expression of α5β1-integrin enhances EboV GP-mediated infection of GD25.
Altered cell migration factors and increased intestinal tumorigenesis in APC1638N/+ mice. Altered cell migration factors and increased intestinal tumorigenesis.

Altered cell migration factors and increased intestinal tumorigenesis in APC1638N/+ mice. Altered cell migration factors and increased intestinal tumorigenesis.
Chick cardiac cells before and during C looping exhibit dominant CW rotation in vitro. Chick cardiac cells before and during C looping exhibit dominant.

Chick cardiac cells before and during C looping exhibit dominant CW rotation in vitro. Chick cardiac cells before and during C looping exhibit dominant.
DHEA(S) and Allo induced the phosphorylation of PKC in serum-deprived PC12 cells. DHEA(S) and Allo induced the phosphorylation of PKC in serum-deprived.

DHEA(S) and Allo induced the phosphorylation of PKC in serum-deprived PC12 cells. DHEA(S) and Allo induced the phosphorylation of PKC in serum-deprived.
Decreased cell polarity and adhesion protein expression after 56Fe radiation. Decreased cell polarity and adhesion protein expression after 56Fe radiation.

Decreased cell polarity and adhesion protein expression after 56Fe radiation. Decreased cell polarity and adhesion protein expression after 56Fe radiation.
PMAIP1/NOXA gene amplification increases DLBCL vulnerability to BCL2 inhibitors. PMAIP1/NOXA gene amplification increases DLBCL vulnerability to BCL2 inhibitors.

PMAIP1/NOXA gene amplification increases DLBCL vulnerability to BCL2 inhibitors. PMAIP1/NOXA gene amplification increases DLBCL vulnerability to BCL2 inhibitors.
Activation of PKC signaling reverses cell chirality in the myocardium before cardiac looping. Activation of PKC signaling reverses cell chirality in the.

Activation of PKC signaling reverses cell chirality in the myocardium before cardiac looping. Activation of PKC signaling reverses cell chirality in the.
DHEA(S) and Allo protected rat chromaffin cells in culture against serum deprivation-induced apoptosis. DHEA(S) and Allo protected rat chromaffin cells.

DHEA(S) and Allo protected rat chromaffin cells in culture against serum deprivation-induced apoptosis. DHEA(S) and Allo protected rat chromaffin cells.
Long-term decrease of IEC migration after 56Fe radiation relative to γ-rays. Long-term decrease of IEC migration after 56Fe radiation relative to γ-rays.

Long-term decrease of IEC migration after 56Fe radiation relative to γ-rays. Long-term decrease of IEC migration after 56Fe radiation relative to γ-rays.
GPR124 promotes cell migration.

GPR124 promotes cell migration.
Impaired lymphatic valve protrusion in Tie2Cre;Piezo1cKO mice.

Impaired lymphatic valve protrusion in Tie2Cre;Piezo1cKO mice.
Heavy-ion radiation decreases expression of key cellular tight junction proteins and alters microtubule dynamics in mouse intestine. Heavy-ion radiation.

Heavy-ion radiation decreases expression of key cellular tight junction proteins and alters microtubule dynamics in mouse intestine. Heavy-ion radiation.
Long-term up-regulation of proliferative markers and down-regulation of cell migration factors along with increased intestinal metaplasia after 56Fe radiation.

Long-term up-regulation of proliferative markers and down-regulation of cell migration factors along with increased intestinal metaplasia after 56Fe radiation.

Similar presentations

Ads by Google