p53 inhibitor pifithrin α hydrobromide  (MedChemExpress)

Journal: Frontiers in Cell and Developmental Biology

Article Title: Follicular fluid-derived exosomal LINC02701 promotes granulosa cell apoptosis through the GRP75–P53 axis in active endometriosis

doi: 10.3389/fcell.2026.1805254

Figure Lengend Snippet: LINC02701 weakens the GRP75–P53 interaction and enhances P53-associated apoptotic signaling. (A) Co-immunoprecipitation (Co-IP) assay validating the interaction between GRP75 and P53 in SVOG cells, with Input, IgG, and GRP75 IP controls shown. (B) Co-IP analysis of the GRP75–P53 interaction in LINC02701-overexpressing (OE) and untreated (WT) SVOG cells, with quantitative analysis of relative P53 expression in the immunoprecipitated fractions. (C) Immunofluorescence staining of P53 in Vector, WT, and OE cells, together with quantitative analysis of relative fluorescence intensity. Relative P53 fluorescence intensity was quantified using ImageJ after background subtraction from four random fields per condition in three independent experiments. Scale bar = 100 μm. (D) qPCR analysis of apoptosis-related genes, including BAX , PUMA , P21 , and BCL2 , in OE and WT cells. (E) Western blot analysis of BAX, PUMA, and P21 protein expression in OE and WT cells, together with densitometric quantification normalized to GAPDH. OE, LINC02701-overexpressing cells; WT, untreated cells; Vector, empty vector control cells; IP-OE, immunoprecipitated fraction from OE cells; IP-WT, immunoprecipitated fraction from WT cells. Error bars represent mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001; ns, not significant.

Article Snippet: To determine whether the pro-apoptotic effect of LINC02701 is mediated through P53 signaling, SVOG cells overexpressing LINC02701 were treated with the P53 inhibitor Pifithrin-α hydrobromide (MedChemExpress, China).

Techniques: Co-Immunoprecipitation Assay, Expressing, Immunoprecipitation, Immunofluorescence, Staining, Plasmid Preparation, Fluorescence, Western Blot, Control

Journal: Frontiers in Cell and Developmental Biology

Article Title: Follicular fluid-derived exosomal LINC02701 promotes granulosa cell apoptosis through the GRP75–P53 axis in active endometriosis

doi: 10.3389/fcell.2026.1805254

Figure Lengend Snippet: Inhibition of P53 attenuates LINC02701-induced apoptosis. (A) Representative flow cytometry plots of apoptosis in WT + vehicle, OE + vehicle, and OE + Pifithrin-α groups. (B) Quantification of apoptotic cells. (C) Western blot analysis of apoptosis-related proteins, including BAX, PUMA, and cleaved caspase-3. (D) Densitometric quantification of Western blot results. WT, untreated cells; OE, LINC02701-overexpressing cells. Error bars represent mean ± SD.

Article Snippet: To determine whether the pro-apoptotic effect of LINC02701 is mediated through P53 signaling, SVOG cells overexpressing LINC02701 were treated with the P53 inhibitor Pifithrin-α hydrobromide (MedChemExpress, China).

Techniques: Inhibition, Flow Cytometry, Western Blot

Journal: Frontiers in Cell and Developmental Biology

Article Title: Follicular fluid-derived exosomal LINC02701 promotes granulosa cell apoptosis through the GRP75–P53 axis in active endometriosis

doi: 10.3389/fcell.2026.1805254

Figure Lengend Snippet: Proposed mechanism by which follicular fluid-derived exosomal LINC02701 promotes granulosa-cell apoptosis in active endometriosis. Exosomal LINC02701 enters granulosa cells, interacts with GRP75, weakens the GRP75–P53 interaction, promotes P53 accumulation, and activates downstream apoptotic signaling.

Article Snippet: To determine whether the pro-apoptotic effect of LINC02701 is mediated through P53 signaling, SVOG cells overexpressing LINC02701 were treated with the P53 inhibitor Pifithrin-α hydrobromide (MedChemExpress, China).

Techniques: Derivative Assay

Journal: Genes

Article Title: CALB2 Expression Is Associated with Tumor Progression and Prognosis in Colorectal Adenocarcinoma

doi: 10.3390/genes17050510

Figure Lengend Snippet: Association of CALB2 expression with p53 signaling in colorectal adenocarcinoma. ( A , B ) Western blot analysis of p-p53-Ser33 and total p53 protein levels ( A ) and corresponding densitometric quantification ( B ) in HCT116 cells following CALB2 knockdown using two independent siRNAs (si1-CALB2 and si2-CALB2) or negative control (NC). ( C , D ) Western blot analysis of p-p53-Ser33 and total p53 protein levels ( C ) and corresponding densitometric quantification ( D ) in HT29 cells after CALB2 knockdown or negative control (NC). ( E , F ) Western blot analysis of p-p53-Ser33 and total p53 protein levels ( E ) and corresponding densitometric quantification ( F ) in SW48 cells after CALB2 overexpression (OE-CALB2) or negative control (NC). ( G , H ) Western blot analysis of p-p53-Ser33 and total p53 protein levels ( G ) and corresponding densitometric quantification ( H ) in SW480 cells after CALB2 overexpression (OE-CALB2) or negative control (NC). ( I – K ) RT-qPCR analysis of CALB2 ( I ), p21(CDKN1A) ( J ), and BAX ( K ) mRNA levels in HCT116 cells transfected with NC, si1-CALB2, or si1-CALB2 combined with the p53 inhibitor PFT-α (10 μM). ( L ) CCK-8 assay of HCT116 cells in the NC, si1-CALB2, and si1-CALB2+PFT-α groups over a 96 h period. ( M , N ) Representative images of scratch wound-healing assays ( M ) and quantitative analysis of relative migration rates ( N ) in HCT116 cells at 0, 24, and 48 h post-scratching. Scale bar = 250 μm. ( O – Q ) Representative double immunofluorescence staining ( O ) and quantitative analysis of fluorescence intensity ( P , Q ) for CALB2 and p-p53-Ser33 in xenograft tumor tissues from NC and OE-CALB2 groups. Scale bar = 50 μm. (n = 3, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Article Snippet: The p53-specific inhibitor PFT-α hydrobromide (PFT-α, 10 μM; MCE, Monmouth Junction, NJ, USA) was introduced to the culture medium 24 h after siRNA transfection.

Techniques: Expressing, Western Blot, Knockdown, Negative Control, Over Expression, Quantitative RT-PCR, Transfection, CCK-8 Assay, Migration, Double Immunofluorescence Staining, Fluorescence

Journal: International Journal of Molecular Sciences

Article Title: Lycium barbarum Glycopeptide Inhibits Colorectal Cancer Cell Proliferation via Activating p53/p21 Pathway and Inducing Cellular Senescence

doi: 10.3390/ijms26157091

Figure Lengend Snippet: Effects of LbGP on p53/p21 expression and cell cycle distribution in CT26 cells. ( A ) Western blot and band intensity quantification of p53 and p21 expression after 72 h of LbGP treatment. Two 0 μg/mL samples were used as technical replicates for both protein blots. GAPDH served as the loading control. ( B ) Flow cytometry analysis of cell cycle distribution at 72 h, showing an increased proportion of cells in S phase and a decreased proportion in G2/M phase. n = 3. * p < 0.05; n.s., not significant compared to the control (0 μg/mL).

Article Snippet: The p53 inhibitor Pifithrin-α hydrobromide was purchased from Selleck Chemicals, Houston, TX, USA (S2929).

Techniques: Expressing, Western Blot, Control, Flow Cytometry

Journal: International Journal of Molecular Sciences

Article Title: Lycium barbarum Glycopeptide Inhibits Colorectal Cancer Cell Proliferation via Activating p53/p21 Pathway and Inducing Cellular Senescence

doi: 10.3390/ijms26157091

Figure Lengend Snippet: LbGP increases p53/p21 expression and reduces tumor cell proliferation in vivo. ( A ) Western blot quantification of p53 and p21 expressions in tumor tissues at day 21. β-actin served as the loading control. ( B ) Immunohistochemistry (IHC) staining and quantification of Ki-67–positive cells in tumor sections (200× and 400×; scale bars = 100 μm and 25 μm, Leica; antibody 1:150). Brown nuclei represent Ki-67–positive cells. n = 8 per group; data represent mean ± SD. * p < 0.05; compared to PBS.

Article Snippet: The p53 inhibitor Pifithrin-α hydrobromide was purchased from Selleck Chemicals, Houston, TX, USA (S2929).

Techniques: Expressing, In Vivo, Western Blot, Control, Immunohistochemistry

Journal: Journal of Cancer Research and Clinical Oncology

Article Title: AR expression-independent XRCC3 mediates DNA damage-induced p53/Bax signaling pathway activation against prostate cancer

doi: 10.1007/s00432-024-05989-8

Figure Lengend Snippet: Effects of silencing XRCC3 on DNA damage-induced p53/Bax signaling pathway in PCa cells. A Accumulation of dsDNA in 22Rv1 cells. B Accumulation of dsDNA in DU145 cells. C Protein bands in nucleus and cytoplasm of 22Rv1 cells. D Protein bands in nucleus and cytoplasm of DU145 cells. E Statistics of XRCC3 and γH2AX expression in 22Rv1 cells. F Statistics of XRCC3 and γH2AX expression in DU145 cells. G Protein bands in cytoplasm of 22Rv1 cells. (H) Protein bands in cytoplasm of DU145 cells. I Statistics of p53 and Bax expression in 22Rv1 cells. J Statistics of p53 and Bax expression in DU145 cells. (*, P < 0.05; **, P < 0.01; ***, P < 0.001)

Article Snippet: Specific p53 inhibitor Pifithrin-α (PFT-α) hydrobromide (MCE, USA) was added at 5, 10, 20, 40, 60, 80 and 100 μM and treated for 48 h. OD values of cells were detected according to CCK-8 method.

Techniques: Expressing

Journal: BMC oral health

Article Title: Effect and mechanism of resveratrol on ferroptosis mediated by p53/SLC7A11 in oral squamous cell carcinoma.

doi: 10.1186/s12903-024-04395-3

Figure Lengend Snippet: Fig. 2 Res induced ferroptosis with up-regulation of p53 in OSCC cells. A: Cell viability was evaluated by CCK-8. B: p53 expression in the nucleus and cytoplasm and GPX4 protein expression were determined by Western blotting; C: The Fe2+ content was detected by the kits; D: The kits were used to detect the ROS level and GSH content. E: LDH release assay was used to evaluate cell death. The cell experiment was performed three times. Data were expressed as mean ± SD. One-way ANOVA was used for data comparison among multiple groups, and Tukey’s test was used for the post-hoc test. ** P < 0.01, *** P < 0.001

Article Snippet: The P53 inhibitor pifithrin-α (PFT-α) was procured from Topscience (Shanghai, China).

Techniques: CCK-8 Assay, Expressing, Western Blot, Lactate Dehydrogenase Assay, Comparison

Journal: BMC oral health

Article Title: Effect and mechanism of resveratrol on ferroptosis mediated by p53/SLC7A11 in oral squamous cell carcinoma.

doi: 10.1186/s12903-024-04395-3

Figure Lengend Snippet: Fig. 3 Downregulation of p53 partially reversed the inhibitory effects of Res on CAL-27 cell malignant behaviors. A: Colony formation experiment was performed to assess colony formation efficiency; B-C: Cell migration and invasion abilities were assessed using the Transwell assay; D: Cell cycle (percent age of cells in G1, S, and G2/M phases) was detected by flow cytometry. The cell experiment was repeated three times, and the data were expressed as mean ± standard deviation. One-way ANOVA was used for comparisons between multiple sets of data, followed by Tukey’s multiple comparisons test. ** P < 0.01, *** P < 0.001

Article Snippet: The P53 inhibitor pifithrin-α (PFT-α) was procured from Topscience (Shanghai, China).

Techniques: Migration, Transwell Assay, Flow Cytometry, Standard Deviation

Journal: BMC oral health

Article Title: Effect and mechanism of resveratrol on ferroptosis mediated by p53/SLC7A11 in oral squamous cell carcinoma.

doi: 10.1186/s12903-024-04395-3

Figure Lengend Snippet: Fig. 4 Res inhibited SLC7A11 transcription by promoting the entry of p53 into the nucleus. A: The mRNA expression of SLC7A11 was detected by RT-qP CR; B: The protein level of SLC7A11 was detected by Western blotting. The cell experiment was performed three times. Data were expressed as mean ± SD. The t test was used for data comparison between the two groups, one-way ANOVA was used for data comparison among multiple groups, and Tukey’s test was used for the post-hoc test. ** P < 0.01, *** P < 0.001

Article Snippet: The P53 inhibitor pifithrin-α (PFT-α) was procured from Topscience (Shanghai, China).

Techniques: Expressing, Western Blot, Comparison

Journal: BMC oral health

Article Title: Effect and mechanism of resveratrol on ferroptosis mediated by p53/SLC7A11 in oral squamous cell carcinoma.

doi: 10.1186/s12903-024-04395-3

Figure Lengend Snippet: Fig. 5 Inhibition of SLC7A11 partly annulled the regulatory effects of p53 silencing on the role of Res in CAL-27 cell malignant behaviors and ferroptosis. A: SLC7A11 and GPX4 protein levels were measured by Western blotting; B: CCK-8 was used to assess cell viability; C: Colony formation experiment was conducted to evaulate colony formation efficiency; D-E: Transwell assay to assess cell migration and invasion abilities; F: Flow cytometry was to detect cell cycle (cell percentages in G1 phase, S phase, and G2/M phase); G: Fe2+ content was assessed by kit; H: The level of ROS and the content of reduced GSH were detected using kits; I: LDH release assay to assess cell death. The cell experiment was repeated three times, and the data were expressed as mean ± standard deviation. One-way ANOVA was used for comparisons between multiple sets of data, followed by Tukey’s multiple comparisons test. ** P < 0.01

Article Snippet: The P53 inhibitor pifithrin-α (PFT-α) was procured from Topscience (Shanghai, China).

Techniques: Inhibition, Western Blot, CCK-8 Assay, Transwell Assay, Migration, Flow Cytometry, Lactate Dehydrogenase Assay, Standard Deviation

Journal: Frontiers in Immunology

Article Title: Altered lipid metabolites accelerate early dysfunction of T cells in HIV-infected rapid progressors by impairing mitochondrial function

doi: 10.3389/fimmu.2023.1106881

Figure Lengend Snippet: The p53 pathway participates in eicosenoate-induced impairment of T-cell mitochondrion function. (A) The top six signaling pathways enriched in 2,317 differentially expressed genes (DEGs) obtained from the analysis of previous transcriptome data (GSE44216) from rapid progressors (RPs) and normal progressors (NPs; adjusted P < 0.05). (B) p53 mRNA expression in PBMCs (GSE44216) was significantly increased in RPs (n = 6) compared with NPs (n = 7) ( P < 0.01). (C) p53 mRNA expression in CD3 + T cells was significantly increased after co-incubation with 500μM eicosenoate and anti-CD3/CD28-coated Dynabeads (4:1 ratio) for 48 h in vitro (n = 7) ( P < 0.05). p53 expression was quantified and normalized to that of GAPDH and expressed using the relative quantification method (2 −ΔΔCt ). (D) Primary CD3 + T cells were stimulated with anti-CD3/CD28-coated Dynabeads (4:1 ratio) and 500μM eicosenoate with or without 20μM p53 inhibitor pifithrin-α and incubated for 24 h, and mitochondrial ROS was detected. The p53 inhibitor pifithrin-α partially reduced the increase in ROS induced by eicosenoate in CD4 + T cells (n = 8). (E) The p53 inhibitor pifithrin-α prevented the increase in ROS induced by eicosenoate in CD8 + T cells to control levels (n = 8). (F) The eicosenoate-induced reduction in mitochondrial mass in CD4 + T cells was not restored by treatment with the p53 inhibitor pifithrin-α (n = 11). (G) The eicosenoate-induced reduction in mitochondrial mass in CD8 + T cells was not restored by treatment with the p53 inhibitor pifithrin-α (n = 11). Representative flow cytograms are shown in each panel. * P < 0.05, ** P < 0.01, and *** P < 0.001. P values were calculated by Mann-Whitney test (B, C) , One-way ANOVA (D) , Friedman test (E–G) . ns, no significance.

Article Snippet: In order to evaluate the effects of p53 on fatty acid eicosenoate-treated T-cell mitochondrial function, primary isolated T cells were co-treated with the p53 inhibitor pifithrin-α (20μM; Santa Cruz Biotechnologies, Santa Cruz, CA, USA) for 24 h ( , ).

Techniques: Protein-Protein interactions, Expressing, Incubation, In Vitro, Quantitative Proteomics, Control, MANN-WHITNEY

Journal: Frontiers in Nutrition

Article Title: Hydroxy-γ-sanshool from Zanthoxylum bungeanum (prickly ash) induces apoptosis of human colorectal cancer cell by activating P53 and Caspase 8

doi: 10.3389/fnut.2022.914638

Figure Lengend Snippet: Primers used for real-time PCR.

Article Snippet: The Caspase 8 inhibitor Z-IETD-FMK and P53 inhibitor PFTα hydrobromide were obtained from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Sequencing

Journal: Frontiers in Nutrition

Article Title: Hydroxy-γ-sanshool from Zanthoxylum bungeanum (prickly ash) induces apoptosis of human colorectal cancer cell by activating P53 and Caspase 8

doi: 10.3389/fnut.2022.914638

Figure Lengend Snippet: Expression of cell-cycle related protein and genes in HCT-116 cells after treatment with hydroxy-γ-sanshool (HRS). (A) Relative mRNA level of related genes in HCT-116 cells. (B) Western blot of effects on HRS on cell-cycle related proteins in HCT-116 cells. (C) Levels of cell-cycle related proteins. (D) Protein level of p53 in HCT-116 cells, with or without a p53 inhibitor (PFTα hydrobromide). HCT-116 cells were treated with HRS at designated concentrations and compared to untreated cells. All data were expressed as means ± SD for three replicated experiments. a− d Within a cluster, columns without a common superscript differed ( p < 0.05).

Article Snippet: The Caspase 8 inhibitor Z-IETD-FMK and P53 inhibitor PFTα hydrobromide were obtained from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Expressing, Western Blot