Journal: Molecular and Cellular Biochemistry

Article Title: TOR1 AIP1 interacts with p53 to enhance cell cycle dysregulation in prostate cancer progression

doi: 10.1007/s11010-025-05276-1

Figure Lengend Snippet: The expression of TOR1 AIP1 was downregulated in prostate cancer samples. A The expression of TOR1 AIP1 in 499 tumor tissues and 52 normal tissues was analyzed by TCGA. B The expression level of TOR1 AIP1 was validated by qPCR using clinical samples ( n = 5). C The protein level of TOR1 AIP1 in human prostate tumor specimens was determined by WB ( n = 3). D The expression of TOR1 AIP1 in prostate cancer was examined by IHC ( n = 3). Normal group: Non-cancerous tissue adjacent to the tumor, Tumor group: neoplastic tissue. Compared with the indicated group, * P < 0.05, ** P < 0.01, and *** P < 0.001

Article Snippet: To further confirm that the p53 expression might serve as the molecular mechanism of TOR1 AIP1 involved in the development of PRAD, we used pifithrin-α (MedChemExpress, Shanghai, China), an inhibitor of p53 protein, to determine if it resulted in rescuing the effect of TOR1 AIP1 on tumor progression.

Techniques: Expressing

Journal: Molecular and Cellular Biochemistry

Article Title: TOR1 AIP1 interacts with p53 to enhance cell cycle dysregulation in prostate cancer progression

doi: 10.1007/s11010-025-05276-1

Figure Lengend Snippet: The prognostic value of TOR1 AIP1 in prostate cancer patients. A The prognostic value of mRNA Level of TOR1 AIP1 in prostate cancer patients (Kaplan–Meier Plotter). B – E Lower TOR1 AIP1 expression was associated with age, N stage, T stage, and M stage. F ROC curve analysis of TOR1 AIP1. Compared with the indicated group, * P < 0.05, ** P < 0.01, and *** P < 0.001

Article Snippet: To further confirm that the p53 expression might serve as the molecular mechanism of TOR1 AIP1 involved in the development of PRAD, we used pifithrin-α (MedChemExpress, Shanghai, China), an inhibitor of p53 protein, to determine if it resulted in rescuing the effect of TOR1 AIP1 on tumor progression.

Techniques: Expressing

Journal: Molecular and Cellular Biochemistry

Article Title: TOR1 AIP1 interacts with p53 to enhance cell cycle dysregulation in prostate cancer progression

doi: 10.1007/s11010-025-05276-1

Figure Lengend Snippet: TOR1 AIP1 inhibited the proliferation and invasion of the DU145 and PC3M cells. TOR1 AIP1 stably overexpression DU145 cells and PC3M cells using lentivirus were generated. A and B The viability of DU145 and PC3M cells were measured by CCK8 assay at the indicated times. C and D Colony formation assays were performed in DU145 cells and PC3M cells transfected with indicated lentivirus. E – G The penetrability in Transwell chambers was measured to verify the invasive capability of DU145 cells and PC3M cells. Data represent mean ± SD ( n = 3). NC: Control virus-transfected cells, TOR1 AIP1 OVE: TOR1 AIP1-overexpressing cells. Compared with the indicated group, * P < 0.05, ** P < 0.01, and *** P < 0.001

Article Snippet: To further confirm that the p53 expression might serve as the molecular mechanism of TOR1 AIP1 involved in the development of PRAD, we used pifithrin-α (MedChemExpress, Shanghai, China), an inhibitor of p53 protein, to determine if it resulted in rescuing the effect of TOR1 AIP1 on tumor progression.

Techniques: Stable Transfection, Over Expression, Generated, CCK-8 Assay, Transfection, Control, Virus

Journal: Molecular and Cellular Biochemistry

Article Title: TOR1 AIP1 interacts with p53 to enhance cell cycle dysregulation in prostate cancer progression

doi: 10.1007/s11010-025-05276-1

Figure Lengend Snippet: shRNA-mediated silencing of TOR1 AIP1 increased the proliferation, migration, and invasion of PRAD cells. TOR1 AIP1 stably knockdown 22RV1 and C4 - 2 cell lines using lentivirus were generated. A and B The viability of 22RV1 and C4 - 2 cells were measured by CCK8 assay at the indicated times. C and D Colony formation assays were performed in 22RV1 and C4 - 2 cells transfected with indicated lentivirus. E – G Transwell assays were used to detect the migration and invasion ability of 22RV1 and C4 - 2 cells. NC: Control virus-transfected cells, sh#1 and sh#2: TOR1 AIP1 knockdown cells. Data represent mean ± SD ( n = 3). By comparison with vehicle control group, * P < 0.05 and *** P < 0.001

Article Snippet: To further confirm that the p53 expression might serve as the molecular mechanism of TOR1 AIP1 involved in the development of PRAD, we used pifithrin-α (MedChemExpress, Shanghai, China), an inhibitor of p53 protein, to determine if it resulted in rescuing the effect of TOR1 AIP1 on tumor progression.

Techniques: shRNA, Migration, Stable Transfection, Knockdown, Generated, CCK-8 Assay, Transfection, Control, Virus, Comparison

Journal: Molecular and Cellular Biochemistry

Article Title: TOR1 AIP1 interacts with p53 to enhance cell cycle dysregulation in prostate cancer progression

doi: 10.1007/s11010-025-05276-1

Figure Lengend Snippet: TOR1 AIP1 overexpression suppressed the progression of PRAD in vivo. We generated TOR1 AIP1 stably overexpressed DU145 cells and PC3M cells (TOR1 AIP1 OVE) or TOR1 AIP1 stably knockdown 22RV1 cells and C4 - 2 cells (sh#1 and sh#2) and control cells (shNC) and injected them subcutaneously into the right axils of nude mice. A and B Xenograft tumor images of DU145 cells and PC3M cells stably transfected with NC or TOR1 AIP1 overexpression. C and D Tumor Weight of DU145 cells and PC3M cells stably transfected with NC or TOR1 AIP1 overexpression ( n = 5). E and F The growth curve of DU145 cells and PC3M cells stably transfected with NC or TOR1 AIP1 overexpression in nude mice ( n = 5). G and H Xenograft tumor images of 22RV1 cells and C4 - 2 cells stably transfected with shNC or TOR1 AIP1 sh#1 and sh#2 ( n = 4). I and J Tumor weight of shNC and TOR1 AIP1 sh#1 and sh#2 ( n = 4). K and L The growth curve of different groups ( n = 4). NC and shNC: Nude mice inoculated with control virus-transfected cells, OVE: Nude mice injected with TOR1 AIP1-overexpressing cells, sh#1 and sh#2: Nude mice injected with TOR1 AIP1 knockdown cells. Data represent mean ± SD. Compared with the indicated group, *** P < 0.001

Article Snippet: To further confirm that the p53 expression might serve as the molecular mechanism of TOR1 AIP1 involved in the development of PRAD, we used pifithrin-α (MedChemExpress, Shanghai, China), an inhibitor of p53 protein, to determine if it resulted in rescuing the effect of TOR1 AIP1 on tumor progression.

Techniques: Over Expression, In Vivo, Generated, Stable Transfection, Knockdown, Control, Injection, Transfection, Virus

Journal: Molecular and Cellular Biochemistry

Article Title: TOR1 AIP1 interacts with p53 to enhance cell cycle dysregulation in prostate cancer progression

doi: 10.1007/s11010-025-05276-1

Figure Lengend Snippet: TOR1 AIP1 interacts with p53 to inhibit the tumor progression in vitro. A – C Cell cycle analysis was performed using flow cytometry. D and E The expressions of p53 protein in DU145 and PC3M cells with stably transfected with NC or TOR1 AIP1 overexpression were determined by western blot. F and G The interaction between TOR1 AIP1 and p53 in DU145 and PC3M cells was determined by CO-IP. H and I The viability of TOR1 AIP1 stably overexpression DU145 cells and PC3M cells with or without pifithrin-α treatment were measured by CCK8 assay. J and K Colony formation assays were performed in TOR1 AIP1 stably overexpression DU145 cells and PC3M cells with or without pifithrin-α treatment. L – N Transwell assay was used to detect the effect of pifithrin-α on migration and invasion of TOR1 AIP1 stably overexpression DU145 cells and PC3M cells. Data represent mean ± SD ( n = 3). NC: Control virus-transfected cells, TOR1 AIP1 OVE: TOR1 AIP1-overexpressing cells. Compared with the indicated group, *** P < 0.001, n.s, no significant difference

Article Snippet: To further confirm that the p53 expression might serve as the molecular mechanism of TOR1 AIP1 involved in the development of PRAD, we used pifithrin-α (MedChemExpress, Shanghai, China), an inhibitor of p53 protein, to determine if it resulted in rescuing the effect of TOR1 AIP1 on tumor progression.

Techniques: In Vitro, Cell Cycle Assay, Flow Cytometry, Stable Transfection, Transfection, Over Expression, Western Blot, Co-Immunoprecipitation Assay, CCK-8 Assay, Transwell Assay, Migration, Control, Virus

Journal: Molecular and Cellular Biochemistry

Article Title: TOR1 AIP1 interacts with p53 to enhance cell cycle dysregulation in prostate cancer progression

doi: 10.1007/s11010-025-05276-1

Figure Lengend Snippet: p53-mediated the anti-tumor effect of TOR1 AIP1 in vivo. We injected subcutaneously TOR1 AIP1 stably overexpression cells, with or without pifithrin-α intratumoral treatment for nude mice. A – F Tumor images ( A , B ), tumor weights ( C , D ), and tumor growth curve ( E , F ) of different groups. Data represent mean ± SD ( n = 5). NC: Nude mice inoculated with control virus-transfected cells, OVE: Nude mice injected with TOR1 AIP1-overexpressing cells. Compared with the indicated group, ** P < 0.01 and *** P < 0.001

Article Snippet: To further confirm that the p53 expression might serve as the molecular mechanism of TOR1 AIP1 involved in the development of PRAD, we used pifithrin-α (MedChemExpress, Shanghai, China), an inhibitor of p53 protein, to determine if it resulted in rescuing the effect of TOR1 AIP1 on tumor progression.

Techniques: In Vivo, Injection, Stable Transfection, Over Expression, Control, Virus, Transfection

Journal:

Article Title: Activation of NF-?B and inhibition of p53-mediated apoptosis by API2/mucosa-associated lymphoid tissue 1 fusions promote oncogenesis

doi: 10.1073/pnas.0402415101

Figure Lengend Snippet: The fusion constructs Fus1 and Fus2 activate NF-κB in a luciferase promoter assay. 293 cells were transfected in triplicate with pcDNA3, pcDNA3-Fus1, pcDNA3-Fus2, pcDNA3-Del, pcDNA3-API2, or pcDNA3-MALT1 in the presence of pTK-Luc (an NF-κB responsive luciferase reporter) and pEF1-BOS-β-gal (used as a control for transfection efficiency). Strong activation of NF-κB levels was observed with the Fus 1 and Fus 2 constructs. However, the MALT1 full-length cDNA and the Del 1 construct failed to activate NF-κB. As expected, the pcDNA3-API2 full-length construct slightly activated NF-κB.

Article Snippet: The API2 construct was kindly provided by Dr. Eric LaCasse (Apoptogen), and the FUS2 construct was provided by Dr. V. Dixit (Genentech). cDNA microarray experiments were performed in the Memorial Sloan-Kettering Cancer Center Core Facility with Dr. Agnes Viale.

Techniques: Construct, Luciferase, Promoter Assay, Transfection, Control, Activation Assay

Journal: International Journal of Molecular Medicine

Article Title: Curcumin attenuates myocardial ischemia-reperfusion-induced autophagy-dependent ferroptosis via Sirt1/AKT/FoxO3a signaling

doi: 10.3892/ijmm.2025.5492

Figure Lengend Snippet: Cur decreases A/R injury in H9c2 cells via Sirt1. Expression of (A) apoptosis-associated proteins in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (B) Relative protein expression of Bcl2. (C) represents the relative protein expression of Bax. Expression of Sirt1 (D) in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (E) Relative protein expression of Sirt1. Apoptosis rate of H9c2 cells was measured by flow cytometry (F and G) illustrates the proportion of apoptotic cells as determined by flow cytometry. (H) caspase 3, (I) LDH activity and (J) viability of A/R injured H9c2 cells after Cur pretreatment, silencing of Sirt1 expression and targeted inhibition of AKT activity. * P<0.05, ** P<0.01, *** P<0.001. Cur, curcumin; A/R, anoxia/reoxygenation; Sirt, silent information regulator 1; LDH, Lactate dehydrogenase; si, small interfering; NC, non-targeting control; API-2, triciribine; CON, control.

Article Snippet: Cur (purity ≥98%, batch no. DC0279-0005) was purchased from Dester Technology Co., Ltd. and Akt inhibitor triciribine (API-2; cat. no. GC15392) was purchased from GLPBIO Technology LLC.

Techniques: Expressing, Inhibition, Activity Assay, Flow Cytometry, Control

Journal: International Journal of Molecular Medicine

Article Title: Curcumin attenuates myocardial ischemia-reperfusion-induced autophagy-dependent ferroptosis via Sirt1/AKT/FoxO3a signaling

doi: 10.3892/ijmm.2025.5492

Figure Lengend Snippet: Cur reduces autophagy-dependent ferroptosis in H9c2 cells associated with A/R injury via Sirt1. Expression of autophagy-(A) and ferroptosis-related proteins (B) in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (C) Relative protein expression of P62 and the ratio of LC3II/I. (D) Relative protein expression of NCOA4 and FTH1. Detection of (E) total iron ions, (F) MDA, (G) GSSG, (H) GSH, (I) GSH/GSSG and (J) SOD in A/R injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. Fluorescence intensity of (K) lysosomes, (L) ROS and (M) Fe 2+ in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity (magnification, ×200; scale bar, 400 μ m). ** P<0.05, *** P<0.01. Cur, curcumin; A/R, anoxia/reoxygenation; Sirt, silent information regulator 1; MDA, malondialdehyde; GSSG, glutathione disulfide; GSH, glutathione; SOD, superoxide dismutase; ROS, reactive oxygen species; NCOA4, nuclear receptor coactivator 4; FTH1, ferritin heavy chain 1; CON, control; si, small interfering; prot, protein; API, triciribine; LC3II, microtubule-associated protein 1 light chain 3 β; NC, non-targeting control.

Article Snippet: Cur (purity ≥98%, batch no. DC0279-0005) was purchased from Dester Technology Co., Ltd. and Akt inhibitor triciribine (API-2; cat. no. GC15392) was purchased from GLPBIO Technology LLC.

Techniques: Expressing, Inhibition, Activity Assay, Fluorescence, Control

Journal: International Journal of Molecular Medicine

Article Title: Curcumin attenuates myocardial ischemia-reperfusion-induced autophagy-dependent ferroptosis via Sirt1/AKT/FoxO3a signaling

doi: 10.3892/ijmm.2025.5492

Figure Lengend Snippet: Cur mediates nuclear localization of FoxO3a via Sirt1/AKT. (A) Western blot analysis of (B) phosphorylation of AKT and FoxO3a in A/R-injured H9c2 cells after Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (C) Western blot analysis of (D) distribution of FoxO3a in the cytoplasm and nucleus of A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. *** P<0.01. Cur, curcumin; PCNA, proliferating cell nuclear antigen; Sirt, silent information regulator 1; A/R, anoxia/reoxygenation; p-, phosphorylated; si, small interfering; NC, non-targeting control; API, Triciribine; CON, control.

Article Snippet: Cur (purity ≥98%, batch no. DC0279-0005) was purchased from Dester Technology Co., Ltd. and Akt inhibitor triciribine (API-2; cat. no. GC15392) was purchased from GLPBIO Technology LLC.

Techniques: Western Blot, Inhibition, Activity Assay, Control