Journal: Technology in Cancer Research & Treatment

Article Title: CCT3 Facilitates the Malignant Progression of NSCLC and SCLC via PI3 K/AKT-EMT Axis and Emerges as a Novel Serum Diagnostic Biomarker

doi: 10.1177/15330338251412203

Figure Lengend Snippet: CCT3 is upregulated in lung cancer tissues and cell lines. (A–F) CCT3 expression in: (A,B) NSCLC ( GSE10072 , GSE19801), (C,D) TCGA-LUAD/LUSC (by stage), (E,F) SCLC ( GSE40419 , GSE30219 ) versus normal tissues (***P < 0.0001); (G) qPCR (left) and Western blot (right) of CCT3 in BEAS-2B versus lung cancer cell lines (GAPDH control, ***P < 0.0001, ns: not significant); (H,I) IHC staining of CCT3 in (H) LUAD and (I) LUSC tissues at 40×/400× magnification.

Article Snippet: Following blocking with 5% BSA, the membranes were incubated overnight at 4 °C with specific primary antibodies: CCT3 (Santa Cruz, sc-271336; 1:200), p-PI3 K (Abmart, T40116 ; 1:500), PI3 K (Abmart, T40115 ; 1:500), p-AKT (Abmart, T40067 ; 1:500), AKT (Proteintech, 10176-2-AP; 1:2000), GAPDH (Proteintech, 60004-1-Ig; 1:5000), Vimentin (Affinity, AF7013; 1:500), E-cadherin (Affinity, AF0131; 1:500), N-cadherin (Affinity, AF5239; 1:500), and SNAI1 (Proteintech, 13099-1-AP; 1:600).

Techniques: Expressing, Western Blot, Control, Immunohistochemistry

Journal: Technology in Cancer Research & Treatment

Article Title: CCT3 Facilitates the Malignant Progression of NSCLC and SCLC via PI3 K/AKT-EMT Axis and Emerges as a Novel Serum Diagnostic Biomarker

doi: 10.1177/15330338251412203

Figure Lengend Snippet: Effects of CCT3 modulation on proliferation, colony formation, and metastasis of lung cancer cells. (A–C) Cell proliferation (CCK-8, A), colony formation (B, images and quantification), and migration/invasion (Transwell, C, images and quantification) in NCI-H1703, DMS114, and NCI-H446 cells transfected with control siRNA (NC), CCT3-targeting siRNAs (si-CCT3#1, si-CCT3#2), empty vector (Vector), or CCT3-overexpressing vector (OE-CCT3); (D) Representative images of xenograft tumors, (E) tumor volume quantification, (F) tumor weight measurement, and (G) IHC analysis of CCT3 and Ki67 expression in tumor tissues from BALB/c nude mice injected with control (shNC) or CCT3-knockdown (shCCT3) NCI-H446 cells; ***P < 0.001, ****P < 0.0001 versus respective controls (NC for siRNA, Vector for OE-CCT3).

Article Snippet: Following blocking with 5% BSA, the membranes were incubated overnight at 4 °C with specific primary antibodies: CCT3 (Santa Cruz, sc-271336; 1:200), p-PI3 K (Abmart, T40116 ; 1:500), PI3 K (Abmart, T40115 ; 1:500), p-AKT (Abmart, T40067 ; 1:500), AKT (Proteintech, 10176-2-AP; 1:2000), GAPDH (Proteintech, 60004-1-Ig; 1:5000), Vimentin (Affinity, AF7013; 1:500), E-cadherin (Affinity, AF0131; 1:500), N-cadherin (Affinity, AF5239; 1:500), and SNAI1 (Proteintech, 13099-1-AP; 1:600).

Techniques: CCK-8 Assay, Migration, Transfection, Control, Plasmid Preparation, Expressing, Injection, Knockdown

Journal: Technology in Cancer Research & Treatment

Article Title: CCT3 Facilitates the Malignant Progression of NSCLC and SCLC via PI3 K/AKT-EMT Axis and Emerges as a Novel Serum Diagnostic Biomarker

doi: 10.1177/15330338251412203

Figure Lengend Snippet: Exploration of CCT3-interacting proteins and downstream signaling pathways in lung cancer. (A) CCT3 protein-protein interaction network (STRING database prediction, Cytoscape visualization; nodes: proteins, edges: interactions); (B) GO enrichment (biological process, cellular component, molecular function) and KEGG pathway analysis of CCT3-interacting proteins (significant enrichment in PI3K-AKT pathway highlighted); (C–E) Western blot analysis of PI3K-AKT pathway components (p-PI3 K, PI3 K, p-AKT, AKT) and EMT markers (N-cadherin, E-cadherin, Vimentin) in NCI-H1703 (C), DMS114 (D), and NCI-H446 (E) cells transfected with control siRNA (NC), CCT3-targeting siRNAs (si-CCT3#1–#2), empty vector (Vector), or CCT3-overexpressing vector (OE-CCT3) (GAPDH loading control).

Article Snippet: Following blocking with 5% BSA, the membranes were incubated overnight at 4 °C with specific primary antibodies: CCT3 (Santa Cruz, sc-271336; 1:200), p-PI3 K (Abmart, T40116 ; 1:500), PI3 K (Abmart, T40115 ; 1:500), p-AKT (Abmart, T40067 ; 1:500), AKT (Proteintech, 10176-2-AP; 1:2000), GAPDH (Proteintech, 60004-1-Ig; 1:5000), Vimentin (Affinity, AF7013; 1:500), E-cadherin (Affinity, AF0131; 1:500), N-cadherin (Affinity, AF5239; 1:500), and SNAI1 (Proteintech, 13099-1-AP; 1:600).

Techniques: Protein-Protein interactions, Western Blot, Transfection, Control, Plasmid Preparation

Journal: Technology in Cancer Research & Treatment

Article Title: CCT3 Facilitates the Malignant Progression of NSCLC and SCLC via PI3 K/AKT-EMT Axis and Emerges as a Novel Serum Diagnostic Biomarker

doi: 10.1177/15330338251412203

Figure Lengend Snippet: Rescue assays confirm PI3K-AKT signaling mediates CCT3-regulated lung cancer cell phenotypes. (A) CCK-8 proliferation curves, (B) colony formation (images and quantification), and (C) migration/invasion (Transwell, images and quantification) in NCI-H1703, DMS114, and NCI-H446 cells transfected with control siRNA (NC), CCT3-targeting siRNA (si_CCT3), or si_CCT3 plus PI3 K agonist 740Y-P (si_CCT3 + 740Y-P); ****P < 0.0001 for si_CCT3 versus NC or si_CCT3 + 740Y-P versus si_CCT3.

Article Snippet: Following blocking with 5% BSA, the membranes were incubated overnight at 4 °C with specific primary antibodies: CCT3 (Santa Cruz, sc-271336; 1:200), p-PI3 K (Abmart, T40116 ; 1:500), PI3 K (Abmart, T40115 ; 1:500), p-AKT (Abmart, T40067 ; 1:500), AKT (Proteintech, 10176-2-AP; 1:2000), GAPDH (Proteintech, 60004-1-Ig; 1:5000), Vimentin (Affinity, AF7013; 1:500), E-cadherin (Affinity, AF0131; 1:500), N-cadherin (Affinity, AF5239; 1:500), and SNAI1 (Proteintech, 13099-1-AP; 1:600).

Techniques: CCK-8 Assay, Migration, Transfection, Control

Journal: Technology in Cancer Research & Treatment

Article Title: CCT3 Facilitates the Malignant Progression of NSCLC and SCLC via PI3 K/AKT-EMT Axis and Emerges as a Novel Serum Diagnostic Biomarker

doi: 10.1177/15330338251412203

Figure Lengend Snippet: CCT3-related functional validation, clinical significance, and mechanistic insights in lung cancer. (A–C) Western blot analysis of PI3 K - AKT pathway proteins (p-PI3 K, PI3 K, p-AKT, AKT) and EMT markers (N-cadherin, E-cadherin, Vimentin) in (A) NCI - H1703, (B) DMS114, and (C) NCI - H446 cells transfected with NC, si_CCT3, or si_CCT3 + 740Y - P. (D–F) Serum CCT3 concentrations in normal controls (NC), pulmonary nodules (PN), non-small cell lung cancer (NSCLC), and small cell lung cancer (SCLC) (**P < 0.01, ***P < 0.001, ****P < 0.0001); CCT3 levels in (E) NSCLC and (F) SCLC patients stratified by tumor stage (I–IV) and lymph node metastasis (N0 vs N1). (G–J) ROC curves: (G) CCT3 alone for PN/NSCLC/SCLC diagnosis; (H–I) Other tumor markers (eg, CEA, NSE) for NSCLC and SCLC diagnosis, respectively; (J) CCT3 combined with other markers for NSCLC/SCLC diagnosis. (K) Bootstrap internal validation (1000 iterations) for the CCT3 diagnostic model. (L–M) Decision-curve analysis (DCA) evaluating the net clinical benefit of CCT3-based models across different threshold probabilities for (L) NSCLC and (M) SCLC. (N) Schematic model summarizing the role of CCT3 in promoting lung cancer proliferation and metastasis via activation of the PI3K-AKT pathway and induction of epithelial-mesenchymal transition (EMT), integrating experimental and clinical findings.

Article Snippet: Following blocking with 5% BSA, the membranes were incubated overnight at 4 °C with specific primary antibodies: CCT3 (Santa Cruz, sc-271336; 1:200), p-PI3 K (Abmart, T40116 ; 1:500), PI3 K (Abmart, T40115 ; 1:500), p-AKT (Abmart, T40067 ; 1:500), AKT (Proteintech, 10176-2-AP; 1:2000), GAPDH (Proteintech, 60004-1-Ig; 1:5000), Vimentin (Affinity, AF7013; 1:500), E-cadherin (Affinity, AF0131; 1:500), N-cadherin (Affinity, AF5239; 1:500), and SNAI1 (Proteintech, 13099-1-AP; 1:600).

Techniques: Functional Assay, Biomarker Discovery, Western Blot, Transfection, Diagnostic Assay, Activation Assay

Journal: Journal of Molecular Histology

Article Title: CCT7 predicts poor prognosis and correlates with immune infiltration in colonic adenocarcinoma

doi: 10.1007/s10735-026-10715-4

Figure Lengend Snippet: CCT7 was upregulated in human COAD tissue. A–F Analyses based on TCGA-COAD ( A) , GSE39582 ( B) , GSE41258 ( C) , GSE37364 ( D) , GSE44076 ( E) and GSE41328 ( F) datasets demonstrated significantly higher CCT7 mRNA expression in COAD cancer tissues than in paracancerous tissues. G and H Increased protein ( G) and mRNA ( H) levels of CCT7 in the COAD cell lines RKO and HCT-116 compared with normal colon cell line NCM460. I Representative images of IHC detection for CCT7 expression in cancerous and paired noncancerous samples obtained from COAD patients. The left image, showing normal colon tissues, indicated that CCT7 was not detected, and the middle and right images demonstrated the low and high expression of CCT7 respectively in COAD tissues. All photomicrographs were captured at × 200 magnification. The data presented are representative of at least three independent experiments, with values expressed as the mean ± SD. Independent-samples t-test, paired-samples t-test and non-parametric tests were used for two-group comparisons, and one-way ANOVA and non-parametric tests were applied for multi-group comparisons. **** P < 0.0001, * P < 0.05

Article Snippet: The membranes were blocked with 10% skim milk at room temperature for 2 h, then incubated overnight at 4 °C with primary antibodies against CCT7 (15,994-1-AP; Proteintech, China) and β-actin (AC026; Abclonal, China).

Techniques: Expressing

Journal: Journal of Molecular Histology

Article Title: CCT7 predicts poor prognosis and correlates with immune infiltration in colonic adenocarcinoma

doi: 10.1007/s10735-026-10715-4

Figure Lengend Snippet: CCT7 overexpression in COAD tissues predicted poor prognosis. A Kaplan–Meier and log-rank were used to analyze the correlation between the expression of CCT7 and the prognosis of COAD patients. B and C Univariate and multivariate Cox regression analyses based upon TCGA-COAD dataset ( B) and COAD clinical specimens ( C) . (MMR: Mismatch Repair Proteins; PostopTreat: Postoperative treatment)

Article Snippet: The membranes were blocked with 10% skim milk at room temperature for 2 h, then incubated overnight at 4 °C with primary antibodies against CCT7 (15,994-1-AP; Proteintech, China) and β-actin (AC026; Abclonal, China).

Techniques: Over Expression, Expressing

Journal: Journal of Molecular Histology

Article Title: CCT7 predicts poor prognosis and correlates with immune infiltration in colonic adenocarcinoma

doi: 10.1007/s10735-026-10715-4

Figure Lengend Snippet: GO-BP enrichment analysis of genes associated with CCT7. A and B The correlation between each gene and CCT7 expression was analyzed using the TCGA-COAD ( A) and GSE39582 ( B) datasets. C and D GO-BP enrichment analysis of CCT7 was conducted using the TCGA-COAD ( C) and GSE39582 ( D) datasets. Spearman was used for correlation. ( rs : correlation coefficient)

Article Snippet: The membranes were blocked with 10% skim milk at room temperature for 2 h, then incubated overnight at 4 °C with primary antibodies against CCT7 (15,994-1-AP; Proteintech, China) and β-actin (AC026; Abclonal, China).

Techniques: Expressing

Journal: Journal of Molecular Histology

Article Title: CCT7 predicts poor prognosis and correlates with immune infiltration in colonic adenocarcinoma

doi: 10.1007/s10735-026-10715-4

Figure Lengend Snippet: Downregulation of CCT7 repressed the proliferation, migration and invasion of COAD cells. A and B mRNA and protein expression levels of CCT7 in the RKO ( A) and HCT-116 ( B) cell lines. C The CCK-8 assay was performed to investigate the proliferation of COAD cells that were transfected with siNC or siCCT7. D Effect of siCCT7 on colony formation of COAD cells. E and F The migration and invasion abilities of RKO ( E ) and HCT-116 cells ( F) were evaluated using Transwell analysis. All photomicrographs were captured at × 200 magnification. The data presented are representative of at least three independent experiments, with values expressed as the mean ± SD. Independent-samples t-test and non-parametric tests were used for two-group comparisons, and two-way ANOVA was applied for multi-group comparisons. **** P < 0.0001, *** P < 0.001, ** P < 0.01, * P < 0.05

Article Snippet: The membranes were blocked with 10% skim milk at room temperature for 2 h, then incubated overnight at 4 °C with primary antibodies against CCT7 (15,994-1-AP; Proteintech, China) and β-actin (AC026; Abclonal, China).

Techniques: Migration, Expressing, CCK-8 Assay, Transfection

Journal: Journal of Molecular Histology

Article Title: CCT7 predicts poor prognosis and correlates with immune infiltration in colonic adenocarcinoma

doi: 10.1007/s10735-026-10715-4

Figure Lengend Snippet: Associations between CCT7 expression and drug sensitivity based on TCGA-COAD dataset. A–G Negative correlations between the sensitivity scores of OSI-027 ( A ), 5-Fluorouracil ( B ), VX-11e ( C ), MK-1775 ( D ), Palbociclib ( E ), Oxaliplatin ( F ), and Vorinostat ( G ) and CCT7 mRNA expression. H–M Positive correlations between the sensitivity scores of AZD6482 ( H ), AZD8186 ( I ), NU7441 ( J ), ZM447439 ( K ), JQ1 ( L ), and Doramapimod ( M ) and CCT7 mRNA expression. Spearman was used for correlation

Article Snippet: The membranes were blocked with 10% skim milk at room temperature for 2 h, then incubated overnight at 4 °C with primary antibodies against CCT7 (15,994-1-AP; Proteintech, China) and β-actin (AC026; Abclonal, China).

Techniques: Expressing

Journal: Journal of Molecular Histology

Article Title: CCT7 predicts poor prognosis and correlates with immune infiltration in colonic adenocarcinoma

doi: 10.1007/s10735-026-10715-4

Figure Lengend Snippet: High CCT7 expression is associated with multiple metabolic pathways and p53 signaling pathway. A and B KEGG enrichment analysis of CCT7 using the TCGA-COAD (A) and GSE39582 (B) datasets

Article Snippet: The membranes were blocked with 10% skim milk at room temperature for 2 h, then incubated overnight at 4 °C with primary antibodies against CCT7 (15,994-1-AP; Proteintech, China) and β-actin (AC026; Abclonal, China).

Techniques: Expressing

Journal: iScience

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

doi: 10.1016/j.isci.2026.114840

Figure Lengend Snippet: CCT3 expression is associated with unfavorable clinical outcomes in clear cell renal carcinoma (ccRCC) (A) Bar graph depicts the protein expression levels of CCT3 in selected cancer types and their respective normal tissues. Data were obtained from the Clinical Proteomic Tumor Analysis Consortium (CPTAC) unpaired sample analysis. (B) Upregulated expression of CCT3 in clear cell renal carcinoma (ccRCC) compared to normal kidney tissues, as determined by the UALCAN online database analysis. (C) Analysis of the impact of CCT3 expression on the p53/Rb pathway in ccRCC, derived from the CPTAC database. (D) Correlation analysis between CCT3 mRNA expression levels and the mRNA expression levels of key genes involved in the p53/Rb pathway (TP53, Rb1, CDK4, and E2F3) using Spearman correlation, as analyzed by GEPIA. (E and F) Kaplan-Meier survival curves illustrating the association between CCT3 expression and overall survival (OS) and progression-free survival (PFS) in patients with ccRCC. Patients were stratified into low and high CCT3 expression groups. Statistical significance is indicated as ∗ p < 0.05, ∗∗ p < 0.01, ∗ p < 0.001, and ns for non-significant differences. Data in A are presented as mean ± standard deviation (SD). Two-tailed Student’s t test.

Article Snippet: CCT3 , Proteintech , Cat#10571-1-AP; RRID: AB_2073658.

Techniques: Expressing, Derivative Assay, Standard Deviation, Two Tailed Test

Journal: iScience

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

doi: 10.1016/j.isci.2026.114840

Figure Lengend Snippet: The depletion of CCT3 impairs the abilities of proliferation, migration, and invasion in ccRCC cells (A) Western blot analysis was performed to assess the protein expression of CCT3 in four pairs of clear cell renal cell carcinoma tissues (T) and their corresponding adjacent normal tissues (N). ( n = 4). (B) The immunohistochemical results of CCT3 in ccRCC and normal renal tissue in the HPA database. (C) Western blot was used to assess the effects of two distinct CCT3 knockdown sequences in 786-O and 769-P cells. (D and E) Wound-healing assay indicates that CCT3 knockdown suppresses the viability of 786-O and 769-P cells. (F and G) Transwell assay indicates impaired abilities of migration and invasion of 769-P and 786-O cells. (H and I) The proliferative abilities of stably CCT3-depleted 769-P and 786-O cells were measured with an EdU staining assay. (Scale bars, 100 μm. Data in C-I are presented as the means ± SDs ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). Two-tailed Student’s t test for A, Student’s t test for C-I.

Article Snippet: CCT3 , Proteintech , Cat#10571-1-AP; RRID: AB_2073658.

Techniques: Migration, Western Blot, Expressing, Immunohistochemical staining, Knockdown, Wound Healing Assay, Transwell Assay, Stable Transfection, Staining, Two Tailed Test

Journal: iScience

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

doi: 10.1016/j.isci.2026.114840

Figure Lengend Snippet: The reduction of CCT3 induces cellular senescence in ccRCC cells (A) Western blot analysis was performed to assess the protein expression of CDK4, CyclinD, p-Rb (Ser807/811), and p21 in CCT3 knockdown cells. (B) The mRNA expression levels of senescence-associated genes, including interleukin 1 A, TNF, CDK2, CDK4, and CDK6 in CCT3-depleted cells were examined by qRT-PCR. (C) Changes of SA-β-gal activity in CCT3-knockdown cells. Data represent the percentage of cells staining positive for SA-β-gal ±SD. (D) Cell cycle analysis calculated the distribution of the cells in G1, S, and G2/M phases. (E) Representative immunofluorescent staining of p21 and p-Rb (Ser807/811) in each cell. (F) Western blot analysis was performed to assess the protein expression of CDK4, CyclinD, p-Rb (Ser807/811), and p21 in CCT3 overexpressed cells. (G) Wound-healing assay indicates that the overexpression of CCT3 enhances the proliferation capacity of A498 cells. (H) The Transwell assay demonstrated that the overexpression of CCT3 enhances the migratory and invasive capabilities of A498 cells. (Scale bars, 100 μm, all data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001). Student’s t test.

Article Snippet: CCT3 , Proteintech , Cat#10571-1-AP; RRID: AB_2073658.

Techniques: Western Blot, Expressing, Knockdown, Quantitative RT-PCR, Activity Assay, Staining, Cell Cycle Assay, Wound Healing Assay, Over Expression, Transwell Assay

Journal: iScience

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

doi: 10.1016/j.isci.2026.114840

Figure Lengend Snippet: Knockdown of XPO1 inhibited the invasion and migration abilities of ccRCC cells (A) The Venn diagram obtained by taking the intersection of the relevant gene sets of CCT3 and RB1 after screening. (B) Expression level of XPO1 in clear cell RCC from the TCGA database. (C) The immunohistochemical results of XPO1 in ccRCC and normal renal tissue in the HPA database. (D) A Kaplan-Meier curve illustrates OS in patients with ccRCC from low and high XPO1 expression groups. (E) The promoter methylation level of XPO1 in KIRC from the TCGA database. (F) Western blot analysis was performed to assess the protein expression of XPO1 in CCT3-depleted cells. (G) Using Spearman correlation analysis, the correlation between Gene CCT3 and XPO1 expression, and the correlation between XPO1 and RB1 expression. (H) Wound-healing assay indicates that XPO1 knockdown suppresses the viability of 786-O and 769-P cells. (I) Transwell assay indicates impaired abilities of migration and invasion of 769-P and 786-O cells. (Scale bars, 100 μm, all data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). Two-tailed Student’s t test for B and E. Student’s t test for F, H, and I.

Article Snippet: CCT3 , Proteintech , Cat#10571-1-AP; RRID: AB_2073658.

Techniques: Knockdown, Migration, Expressing, Immunohistochemical staining, Methylation, Western Blot, Wound Healing Assay, Transwell Assay, Two Tailed Test

Journal: iScience

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

doi: 10.1016/j.isci.2026.114840

Figure Lengend Snippet: CCT3 regulates RB1 activity by influencing the stability of the XPO1 protein (A) The Co-IP was performed to analyze the endogenous interaction between CCT3 and XPO1 in ccRCC cells. protein pellets were analyzed by Western blot with anti-CCT3 and anti-XPO1 antibodies. (B) Pull-down of CCT3, XPO1, and CCT3 with GST-tagged was analyzed by Western Blot. (C) Western blot analysis of XPO1 in control or CCT3–knockdown cells treated with CHX for the times indicated. (D) Western blot analysis of XPO1 in control or CCT3–knockdown cells treated with BafA1. (E) Western blot analysis of XPO1 in control or CCT3–knockdown cells treated with MG132. (F) Visualization results of the CCT3 and XPO1 molecular docking. (All data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001). One-way ANOVA for C, Student’s t test for D and E.

Article Snippet: CCT3 , Proteintech , Cat#10571-1-AP; RRID: AB_2073658.

Techniques: Activity Assay, Co-Immunoprecipitation Assay, Western Blot, Control, Knockdown

Journal: iScience

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

doi: 10.1016/j.isci.2026.114840

Figure Lengend Snippet: Rescue experiments demonstrate the effects of CCT3 overexpression and XPO1 knockdown on cell function (A) Western blot was used to detect the expression of RB1 and Cyclin D in nuclear and cytoplasmic fractions of cells. (B) Western blot analysis was performed to assess the protein expression of Cyclin D, p-Rb (Ser807/811) in the rescue assay. (C) Senescence β-Galactosidase Staining in rescue assay. (D) A healing assay was performed in the rescue assay. (E) Transwell assay was performed in the rescue assay. (Scale bars, 100 μm, all data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001). One-way ANOVA for D, E.

Article Snippet: CCT3 , Proteintech , Cat#10571-1-AP; RRID: AB_2073658.

Techniques: Over Expression, Knockdown, Cell Function Assay, Western Blot, Expressing, Rescue Assay, Staining, Transwell Assay

Journal: iScience

Article Title: CCT3-mediated regulation of XPO1/RB1 axis stability promotes cellular senescence and tumor progression in clear cell renal carcinoma

doi: 10.1016/j.isci.2026.114840

Figure Lengend Snippet: Knockdown of CCT3 combined with a selective XPO1 inhibitor can promote cellular senescence to suppress tumor progression in vivo (A) Nude mice were used to establish a tumor xenograft model utilizing CCT3 knockdown cell lines and the selective XPO1 inhibitor, Selinexor. (B and C) The tumor volumes and tumor weight of each group. (D) Western blot analysis was performed to assess the protein expression of p53, Cyclin D, CDK4, and PCNA in tissue. (E and F) The immunohistochemistry and immunofluorescence assays of Ki67. (Scale bars, 100 μm. All data were shown as the mean ± SD ( n = 3 per group), ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001). Repeated measures ANOVA for B and C. One-way ANOVA for D and E.

Article Snippet: CCT3 , Proteintech , Cat#10571-1-AP; RRID: AB_2073658.

Techniques: Knockdown, In Vivo, Western Blot, Expressing, Immunohistochemistry, Immunofluorescence