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1.
Figure 2

Figure 2. p53 suppresses EMT phenotype and stem cell properties. From: p53 regulates epithelial-mesenchymal transition (EMT) and stem cell properties through modulating miRNAs.

(a) Images of the cell morphology of MCF12A p53 knocked-down (scale bar: 20 μm). (b) Protein expression levels of MCF12A p53 knocked-down cells. (c) Flow plots showing E-cadherin expression in sorted HMEC-Snail cells expressing GFP-p53 (circle) (n=3, asterisk indicates P<0.05). (d) Flow plots showing percentage of CD24CD44+ population (lower right box) in MCF12A p53 knocked-down cells (n=3, asterisk indicates P<0.05). (e) Flow charts showing the percentage of CD24CD44+ population (lower right box) in sorted HMEC-Snail cells expressing GFP-p53 (circle) (n=3, asterisk indicates P<0.05). Error bars denote ±SD.

Chun-Ju Chang, et al. Nat Cell Biol. ;13(3):317-323.
2.
Figure 3

Figure 3. p53 suppresses EMT phenotype and stem cell properties through upregulating miR-200c. From: p53 regulates epithelial-mesenchymal transition (EMT) and stem cell properties through modulating miRNAs.

(a) miRNA or mRNA expression levels in MCF12A cells expressing the indicated constructs (n=4, asterisk indicates P<0.05). (b) The percentage of CD24CD44+ population in MCF12A cells expressing the indicated constructs (n=3, asterisk indicates P<0.05). (c) Images showing mammosphere formation in MCF12A cells expressing the indicated constructs. Number of spheres were counted for 10 fields in each group (scale bar: 100 μm, n=3, asterisk indicates P<0.05). (d) Flow plots showing E-cadherin expression in HMEC-Snail cells expressing the indicated constructs (n=3, asterisk indicates P<0.05). (e) miRNA or mRNA expression levels in HMEC-Snail cells expressing the indicated constructs (n=4, asterisk indicates P<0.05). (f) The percentage of CD24CD44+ population in HMEC-Snail cells expressing the indicated constructs (n=3, asterisk indicates P<0.05). Error bars denote ±SD.

Chun-Ju Chang, et al. Nat Cell Biol. ;13(3):317-323.
3.
Figure 4

Figure 4. Mutated p53 competes with wild-type p53 in the regulation of EMT and stemness markers. From: p53 regulates epithelial-mesenchymal transition (EMT) and stem cell properties through modulating miRNAs.

(a) Protein expression levels of MCF12A cells expressing the indicated constructs. (b) miRNA-200c expression levels of MCF12A cells expressing the indicated constructs (n=4, asterisk indicates P<0.05). (c) The percentage of CD24CD44+ population in MCF12A cells expressing the indicated constructs (n=3, asterisk indicates P<0.05). (d) The percentage of the bound chromatin over input chromatin immunoprecipitated by p53 antibody in MCF12A cells expressing the indicated constructs. IgG was used as a negative control (n=3, asterisk indicates P<0.05). (e) Protein expression levels of BT-549 breast cancer cells expressing the indicated constructs. (f) Fold change in miRNA-200c expression level in BT-549 cells expressing the indicated constructs (n=4, asterisk indicates P<0.05). Error bars denote ±SD.

Chun-Ju Chang, et al. Nat Cell Biol. ;13(3):317-323.
4.
Figure 1

Figure 1. p53 transcriptionally activates miR-183 and miR-200c. From: p53 regulates epithelial-mesenchymal transition (EMT) and stem cell properties through modulating miRNAs.

(a) miRNA expression in isolated CD24CD44+ and non-CD24CD44+ HMEC cells (n=3, double asterisk indicates P<0.01, single asterisk indicates P<0.05). (b) Diagram showing the promoter regions of miR-183 and miR-200c with the putative p53 response elements (p53-RE), and the structure of wild-type and p53RE-mutant luciferase reporters driven by the indicated promoters. (c) The percentage of the bound chromatin/input chromatin using p53 antibody targeting p53 binding elements (A–E) in HMEC cells. IgG was used as a negative control. (n=3, asterisk indicates P<0.05). (d) ChIP-PCR gel (left) and the percentage (right) of the bound chromatin/input chromatin using p53 antibody in MCF12A cells (n=3, asterisk indicates P<0.05). (e) The fold change of luciferase activity driven by wild-type and mutant p53 response elements under etoposide treatment (n=5, asterisk indicates P<0.05). (fg) miRNA or mRNA expression levels in cells expressing the indicated constructs (n=4, asterisk indicates P<0.05). Insets showing p53 protein expression levels. Error bars denote ±SD.

Chun-Ju Chang, et al. Nat Cell Biol. ;13(3):317-323.
5.
Figure 5

Figure 5. Loss of p53 correlates with reduced miR-200c and enhanced ZEB1 and BMI1 expression levels. From: p53 regulates epithelial-mesenchymal transition (EMT) and stem cell properties through modulating miRNAs.

(a) RT-PCR products validate the deletion of p53 (exon2) in p53 knock-out mice. (b) Protein expression levels p53 wild-type (WT1 and WT2) and p53 knock-out mice (KO1 and KO2) mammary cells. KO1-1 and KO1-2 represent samples of two mammary glands collected from the same mouse. (c) Fold change in miRNA or mRNA expression level of mammary cells from the p53 wild-type and p53 knock-out mice (n=3, asterisk indicates p<0.05). Error bars denote ±SD. (d) Representative cases from 106 breast cancer specimens in tissue microarrays were analyzed by immunohistochemical staining (p53, E-cadherin, ZEB1, BMI1) and in situ hybridization (miR-200c) (scale bar: 20 μm). (e) (f) Tables summarizing Chi-Square analysis of immunohistochemical staining results. (−): negative, (+): positive. (g) A proposed model of p53 regulation on epithelial phenotype and stemness through activating miR-200c.

Chun-Ju Chang, et al. Nat Cell Biol. ;13(3):317-323.

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