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ABclonal Biotechnology elf3
Targeted therapy generates distinct SOX9 High stem cell‐like state epithelia. A,B) Pseudotime cell trajectories analysis using Monocle 2 to study the epithelial cellular dynamic changes as PCa progression. A) Visualization in state or B) Seurat cluster. Club cells located in the branching point of the pseudo‐time trajectory map. C,D) Club cell subsets illustrated in C) UMAP plot and D) in violin plots. PIGR, MGP, and MMP7 are canonical club cell markers. The OLFM4 + CSCs showed a characteristic expression of PSCA and OLFM4. E) Stack graph showed the SOX9 High epithelial subset predominantly contributed by PCa‐4 patients. F,I) Depict the epithelial subset composition in situ. Overview of the epithelial composition in F) PCa‐4 and H) PCa‐2 patients. Spatial transcriptomics profile revealed the SOX9 high Club cells and OLFM4 + CSCs share a similar transcriptomic landscape but separate in spatial position. J) Pseudotime trajectory analysis results indicated SOX9 and KLF5 over‐activation might be the driver of normal luminal cell dedifferentiation to cancer stem cells. MYC may be another accelerator that fuels luminal cells to differentiate into cancer epithelial cells. K) Hallmark pathways analysis suggested the SOX9 High epithelial subset enrichment in HALLMARK_EPITHELIAL_MESENCHYMAL_TRANSITION and HALLMARK_WNT_BETA_CATENIN_SIGNALING pathway. L,M) Western blot results suggested that SOX9 or KLF5 over‐activation confers 22Rv1 and RWPE‐1 cell lines with stemness. MYC and CTNNB1 were significantly activated after SOX9 or KLF5 over‐activation in RWPE‐1 cell line. Western blot analysis of cell lysates was performed using antibodies against KRT13, WNT7A, TMPRSS2, MYC, CTNNB1, KLF5, <t>ELF3,</t> SOX9, and ACTIN. N) SOX9 or KLF5 over‐activation drives nuclear β‐catenin localization. Scale bar: 50 µm. O) ChIP‐PCR and P) ChIP‐Seq results suggested CTNNB1 is the direct target of SOX9 and KLF5.
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Image Search Results


Targeted therapy generates distinct SOX9 High stem cell‐like state epithelia. A,B) Pseudotime cell trajectories analysis using Monocle 2 to study the epithelial cellular dynamic changes as PCa progression. A) Visualization in state or B) Seurat cluster. Club cells located in the branching point of the pseudo‐time trajectory map. C,D) Club cell subsets illustrated in C) UMAP plot and D) in violin plots. PIGR, MGP, and MMP7 are canonical club cell markers. The OLFM4 + CSCs showed a characteristic expression of PSCA and OLFM4. E) Stack graph showed the SOX9 High epithelial subset predominantly contributed by PCa‐4 patients. F,I) Depict the epithelial subset composition in situ. Overview of the epithelial composition in F) PCa‐4 and H) PCa‐2 patients. Spatial transcriptomics profile revealed the SOX9 high Club cells and OLFM4 + CSCs share a similar transcriptomic landscape but separate in spatial position. J) Pseudotime trajectory analysis results indicated SOX9 and KLF5 over‐activation might be the driver of normal luminal cell dedifferentiation to cancer stem cells. MYC may be another accelerator that fuels luminal cells to differentiate into cancer epithelial cells. K) Hallmark pathways analysis suggested the SOX9 High epithelial subset enrichment in HALLMARK_EPITHELIAL_MESENCHYMAL_TRANSITION and HALLMARK_WNT_BETA_CATENIN_SIGNALING pathway. L,M) Western blot results suggested that SOX9 or KLF5 over‐activation confers 22Rv1 and RWPE‐1 cell lines with stemness. MYC and CTNNB1 were significantly activated after SOX9 or KLF5 over‐activation in RWPE‐1 cell line. Western blot analysis of cell lysates was performed using antibodies against KRT13, WNT7A, TMPRSS2, MYC, CTNNB1, KLF5, ELF3, SOX9, and ACTIN. N) SOX9 or KLF5 over‐activation drives nuclear β‐catenin localization. Scale bar: 50 µm. O) ChIP‐PCR and P) ChIP‐Seq results suggested CTNNB1 is the direct target of SOX9 and KLF5.

Journal: Advanced Science

Article Title: Integration Analysis of Single‐Cell Multi‐Omics Reveals Prostate Cancer Heterogeneity

doi: 10.1002/advs.202305724

Figure Lengend Snippet: Targeted therapy generates distinct SOX9 High stem cell‐like state epithelia. A,B) Pseudotime cell trajectories analysis using Monocle 2 to study the epithelial cellular dynamic changes as PCa progression. A) Visualization in state or B) Seurat cluster. Club cells located in the branching point of the pseudo‐time trajectory map. C,D) Club cell subsets illustrated in C) UMAP plot and D) in violin plots. PIGR, MGP, and MMP7 are canonical club cell markers. The OLFM4 + CSCs showed a characteristic expression of PSCA and OLFM4. E) Stack graph showed the SOX9 High epithelial subset predominantly contributed by PCa‐4 patients. F,I) Depict the epithelial subset composition in situ. Overview of the epithelial composition in F) PCa‐4 and H) PCa‐2 patients. Spatial transcriptomics profile revealed the SOX9 high Club cells and OLFM4 + CSCs share a similar transcriptomic landscape but separate in spatial position. J) Pseudotime trajectory analysis results indicated SOX9 and KLF5 over‐activation might be the driver of normal luminal cell dedifferentiation to cancer stem cells. MYC may be another accelerator that fuels luminal cells to differentiate into cancer epithelial cells. K) Hallmark pathways analysis suggested the SOX9 High epithelial subset enrichment in HALLMARK_EPITHELIAL_MESENCHYMAL_TRANSITION and HALLMARK_WNT_BETA_CATENIN_SIGNALING pathway. L,M) Western blot results suggested that SOX9 or KLF5 over‐activation confers 22Rv1 and RWPE‐1 cell lines with stemness. MYC and CTNNB1 were significantly activated after SOX9 or KLF5 over‐activation in RWPE‐1 cell line. Western blot analysis of cell lysates was performed using antibodies against KRT13, WNT7A, TMPRSS2, MYC, CTNNB1, KLF5, ELF3, SOX9, and ACTIN. N) SOX9 or KLF5 over‐activation drives nuclear β‐catenin localization. Scale bar: 50 µm. O) ChIP‐PCR and P) ChIP‐Seq results suggested CTNNB1 is the direct target of SOX9 and KLF5.

Article Snippet: ChIP Antibodies: SOX9 (Abclonal, A19710), KLF5 (Abclonal, A2989), ELF3 (Abclonal, A5236).

Techniques: Expressing, In Situ, Activation Assay, Western Blot, ChIP-sequencing

Journal: iScience

Article Title: Versatile roles of annexin A4 in clear cell renal cell carcinoma: Impact on membrane repair, transcriptional signatures, and composition of the tumor microenvironment

doi: 10.1016/j.isci.2025.112198

Figure Lengend Snippet:

Article Snippet: hELF3 (NM_004433) in pLenti C-Myc-DDK-P2A-Puro , OriGene Technologies , RC200631L3.

Techniques: Virus, Generated, Recombinant, Membrane, Electron Microscopy, Saline, Enzyme-linked Immunosorbent Assay, Bicinchoninic Acid Protein Assay, Western Blot, RNA Sequencing, Gene Expression, Imaging, Plasmid Preparation, shRNA, Control, Luciferase, Cloning, Expressing, Software, Cell Analysis, Microscopy, Cell Culture