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Journal: Cancer Pathogenesis and Therapy
Article Title: Neuroendocrine prostate cancer (NEPC)-associated CEP55 promotes cisplatin resistance in prostate cancer by regulating CDK1 phosphorylation
doi: 10.1016/j.cpt.2025.06.008
Figure Lengend Snippet: CEP55 plays an oncogenic role in prostate cancer. (A) The transcript levels of CEP55 in 22 paired prostate tumors and adjacent tissues. (B) The protein level of CEP55 in 4 paired prostate tumors and adjacent tissues. (C) The immunohistochemical picture of 2 paired prostate tumors and adjacent tissues. The scale on the lower left corner represented 100 μm. (D) The protein level of CEP55 in Lncap, C4-2, DU145, and PC3 cells. (E) The translation validation after CEP55 overexpression and knockdown in PC3 cells. (F–K) Cell viability, clone formation, migration, and analysis about DU145, PC3 cells after CEP55 knockdown (F–H) and overexpression (I–K). The scale on the lower right corner represented 200 μm. (L) Subcutaneous tumor formation in nude mice after injecting 1×10 7 shNC or sh CEP55 -1 PC3 cells. The tumor volume was measured every week. Data are represented as mean ± SD. (M) The protein levels of CEP55 , CHGA , NSE , and SYP after CEP55 overexpression in DU145, PC3 cells. (N) The protein levels of CEP55 , CHGA , NSE , and SYP after CEP55 knockdown in PC3 cells. GAPDH acted as an internal reference. ns-not significant difference, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. CEP55 : Centrosomal protein 55; sh CEP55 : Knockdown of CEP5 5 by shRNA; oeCEP55: Overexpression of CEP55; si CEP55 : Small interfering RNA targeting CEP55 ; A 450 : Optical Density at 450 nm; CHGA : Chromogranin A gene; NSE : Neuron-Specific Enolase; SYP : Synaptophysin.
Article Snippet:
Techniques: Immunohistochemical staining, Biomarker Discovery, Over Expression, Knockdown, Migration, shRNA, Small Interfering RNA
Journal: Cancer Pathogenesis and Therapy
Article Title: Neuroendocrine prostate cancer (NEPC)-associated CEP55 promotes cisplatin resistance in prostate cancer by regulating CDK1 phosphorylation
doi: 10.1016/j.cpt.2025.06.008
Figure Lengend Snippet: CEP55 mediated cisplatin resistance via CDK1 phosphorylation at Tyr15 in prostate cancer cells. (A) Relative cell survival rate after CEP55 knockdown and overexpression in DU145 and PC3 cells treated with 1 μg/mL cisplatin for 24 h or not. (B–D) GSEA, GO, and KEGG analyses after being divided into low- and high- CEP55 expression groups from the TCGA database. (E) KEGG analysis of RNA sequencing in shNC and sh CEP55 -2 PC3 cells. (F) Cell cycle assessment of in shNC, sh CEP55 DU145, and PC3 cells treated with 1 μg/mL cisplatin for 24 h. (G) Analysis of co-immunoprecipitation between CEP55 and phospho-CDK1 Tyr15 in DU145, PC3 cells. The IgG group acted as a negative control. (H) The protein level of CEP55 , CDK1, and phospho-CDK1 Tyr15 in shNC, sh CEP55 -2 DU145 cells treated with 1 μg/mL cisplatin for 0, 8, 16, and 24 h. Data are represented as mean ± SD. ns-not significant difference, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. CEP55 : Centrosomal protein 55; sh CEP55 : Knockdown of CEP5 5 by shRNA; oeCEP55: Overexpression of CEP55; si CEP55 : Small interfering RNA targeting CEP55 ; GO: Gene Ontology; KEGG: Kyoto Encyclopedia of Genes and Genomes; GSEA: Gene Set Enrichment Analysis; CDK1: Cyclin-dependent kinase 1; Tyr15: Tyrosine 15.
Article Snippet:
Techniques: Phospho-proteomics, Knockdown, Over Expression, Expressing, RNA Sequencing, Immunoprecipitation, Negative Control, shRNA, Small Interfering RNA
Journal: bioRxiv
Article Title: The natural flavonoid dihydromyricetin targets senescent cells via PRDX2 and alleviates age-related diseases
doi: 10.64898/2025.12.25.696450
Figure Lengend Snippet: ( a ) Schematic of a preclinical treatment procedure. Two weeks after subcutaneous inoculation and in vivo uptake of PC3/PSC27 cell recombinants, NOD/SCID mice received either single-agent or combinatorial metronomic treatment in multiple cycles. ( b ) Tumor end volume analysis. PC3 cells were inoculated alone or with PSC27 cells for subcutaneous implantation at mouse hind flanks, followed by 0.2 mg/kg mitoxantrone (MIT) and 20 mg/kg DMY treatment (single or combined). Left, comparative statistics. Right, representative tumor images. ( c ) Transcriptional analysis of typical SASP factors in stromal and cancer cells isolated via laser capture microdissection (LCM). Signals were normalized to the lowest value of placebo group. ( d ) Transcriptional analysis of two canonical senescence biomarkers p16 Ink4a and p21 Cip1 . ( e ) SA-β-Gal staining in tumor tissue at the end of therapeutic regimens. Left, representative images. Right, comparative statistics. Scale bar, 100 μm. ( f ) Apoptosis assessment via cleaved caspase 3-based immunohistochemistry staining of tumor tissues at the end of therapeutic regimen. Top, representative images. bottom, comparative statistics. Scale bar, 100 μm. ( g ) lmmunohistochemical staining of IL6 in tumor tissues at the end of therapeutic regimen. Left, representative images. Right, comparative statistics. Scale bar, 50 μm. ( i ) Circulating levels of SASP factors including AREG and IL6 in the serum of MIT/DMY-treated NOD/SCID mice. Data are presented as mean ± SD. P values were calculated using Student’s t -tests. ^, P > 0.05; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.
Article Snippet: The
Techniques: In Vivo, Isolation, Laser Capture Microdissection, Staining, Immunohistochemistry
Journal: Frontiers in Medicine
Article Title: Qiling decoction enhances the anti-tumor activity of abiraterone acetate by up-regulating miR-143 expression in abiraterone acetate-resistant prostate cancer cells
doi: 10.3389/fmed.2025.1643506
Figure Lengend Snippet: Dysregulation of miR-143/JNK/p-Bcl2-Beclin1 axis in abiraterone acetate-resistant prostate cancer cells. (A) PC3, abiraterone acetate-resistant PC3 (PC3-AbiR), (B) DU145 and abiraterone acetate-resistant DU145 (DU145-AbiR) cells were incubated with indicated increasing concentrations of abiraterone acetate for 24 h, followed by CCK-8 assay to assess the cell viability. (C) DU145, DU145-AbiR, and (D) PC3 and PC3-AbiR were prepared for qRT-PCR to assess the expression of miR-143. (E) PC3, PC3-AbiR, DU145 and DU145-AbiR cells were lysed for Western blot to assess the protein levels of p-JNK, p-Bcl2 and Beclin1, and (F–K) the optical density analyses were also measured. GAPDH was used as a loading control. Data were presented as the mean ± SD of three independent experiments. ** p < 0.01, **** p < 0.0001.
Article Snippet:
Techniques: Incubation, CCK-8 Assay, Quantitative RT-PCR, Expressing, Western Blot, Control
Journal: Frontiers in Medicine
Article Title: Qiling decoction enhances the anti-tumor activity of abiraterone acetate by up-regulating miR-143 expression in abiraterone acetate-resistant prostate cancer cells
doi: 10.3389/fmed.2025.1643506
Figure Lengend Snippet: miR-143 modulates JNK/p-Bcl2-Beclin1 axis in abiraterone acetate-resistant prostate cancer cells. The miR-143 mimics, miR-143 inhibitor and corresponding control (NC) were respectively transfected into PC3-AbiR cells for 48 h. (A) The cells were then lysed for Western blot to assess the expression of p-JNK, p-Bcl2, Beclin1 and GAPDH, and (B–G) the optical density analyses were also measured. (H) PC3-AbiR cells transfected with NC or miR-143 mimics were incubated with vehicle or 5 ng/ml JNK agonist Anisomycin (ANI) for 24 h, followed by co-immunoprecipitation to assess the binding of p-Bcl2 and Beclin1 complex. IP, immunoprecipitation. IB, immunoblotting. Data were presented as the mean ± SD of three independent experiments. ** p < 0.01, *** p < 0.001.
Article Snippet:
Techniques: Control, Transfection, Western Blot, Expressing, Incubation, Immunoprecipitation, Binding Assay
Journal: Frontiers in Medicine
Article Title: Qiling decoction enhances the anti-tumor activity of abiraterone acetate by up-regulating miR-143 expression in abiraterone acetate-resistant prostate cancer cells
doi: 10.3389/fmed.2025.1643506
Figure Lengend Snippet: Qiling decoction (QLD) enhances the effects of abiraterone acetate on modulating miR-143 expression in abiraterone acetate-resistant prostate cancer cells. (A) PC3-AbiR and (B) DU145-AbiR cells were incubated with 10 mg/mL Qiling decoction (QLD) or 5 μM abiraterone acetate (Abi) for 24 h, followed by CCK-8 assay to assess cell viability. (C,D) Above cells were also prepared for qRT-PCR to assess the expression of miR-143. Data were presented as the mean ± SD of three independent experiments. *** p < 0.001.
Article Snippet:
Techniques: Expressing, Incubation, CCK-8 Assay, Quantitative RT-PCR
Journal: Frontiers in Medicine
Article Title: Qiling decoction enhances the anti-tumor activity of abiraterone acetate by up-regulating miR-143 expression in abiraterone acetate-resistant prostate cancer cells
doi: 10.3389/fmed.2025.1643506
Figure Lengend Snippet: Qiling decoction (QLD) enhances the effects of abiraterone acetate on modulating JNK/p-Bcl2-Beclin1 axis in abiraterone acetate-resistant prostate cancer cells. PC3-AbiR cells were incubated with 10 mg/mL Qiling decoction (QLD) or 5 μM abiraterone acetate (Abi) for 24 h, followed by panel (A) Western blot to assess the protein levels of p-JNK, p-Bcl2 and Beclin1, and (B) the optical density analyses were also measured (B–D). GAPDH was used as a loading control. PC3-AbiR cells were incubated with 10 mg/mL QLD or 5 μM Abi for 24 h, followed by panel (E) co-immunoprecipitation to assess the binding of p-Bcl2 and Beclin1 complex, and (F) the optical density analyses were also measured. IP, immunoprecipitation. IB, immunoblotting. Data were presented as the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01.
Article Snippet:
Techniques: Incubation, Western Blot, Control, Immunoprecipitation, Binding Assay
Journal: Frontiers in Medicine
Article Title: Qiling decoction enhances the anti-tumor activity of abiraterone acetate by up-regulating miR-143 expression in abiraterone acetate-resistant prostate cancer cells
doi: 10.3389/fmed.2025.1643506
Figure Lengend Snippet: Inhibiting miR-143 abolishes the effects of QLD in abiraterone acetate-resistant prostate cancer cells. (A) PC3-AbiR and (B) DU145-AbiR cells were transfected with miR-143 inhibitor or normal control (NC) for 24 h, followed by qRT-PCR to assess the expression of miR-143. (C) PC3-AbiR and (D) DU145-AbiR cells transfected with NC or miR-143 inhibitor were incubated with 10 mg/mL QLD or 5 μM abiraterone acetate (Abi) for 24 h, followed by CCK-8 assay. PC3-AbiR cells transfected with NC or miR-143 inhibitor were incubated with 10 mg/mL QLD or 5 μM Abi for 24 h, followed by panel (E) co-immunoprecipitation to assess the binding of p-Bcl2 and Beclin1 complex, and (F) the optical density analyses were also measured. (G) The mechanism diagram illustrating how QLD induces prostate cancer (PC) cells to overcome abiraterone resistance. Data were presented as the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
Article Snippet:
Techniques: Transfection, Control, Quantitative RT-PCR, Expressing, Incubation, CCK-8 Assay, Immunoprecipitation, Binding Assay