Journal: Journal of Medical Virology

Article Title: SARS‐CoV‐2 pseudovirus infectivity and expression of viral entry‐related factors ACE2, TMPRSS2, Kim‐1, and NRP‐1 in human cells from the respiratory, urinary, digestive, reproductive, and immune systems

doi: 10.1002/jmv.27244

Figure Lengend Snippet: Cell lines used in the present study

Article Snippet: 769‐P , Renal cell adenocarcinoma , ATCC CRL‐1933 , RPMI‐1640 complete medium.

Techniques: Cell Culture

Journal: Cell Death & Disease

Article Title: MAGI3 deficiency unleashes β-catenin conformational change to drive metastatic progression and mTOR inhibitor resistance in ccRCC

doi: 10.1038/s41419-026-08563-x

Figure Lengend Snippet: A Analysis of metastasis-related upregulated gene sets enriched in ccRCC specimens with low MAGI3 expression. Gene expression data from TCGA or GSE73731 were subjected to GSEA to identify pathways associated with metastasis. B Validation of stable MAGI3 overexpression or knockdown in 786-O and 769-P cells using western blotting. C Ectopic expression of MAGI3 suppresses migration in 786-O and 769-P cells. D Knockdown of MAGI3 promotes migration in 786-O and 769-P cells, demonstrated by in vitro scratch assay. E Overexpression of MAGI3 inhibits migration and invasion in 786-O and 769 cells. F Knockdown of MAGI3 promotes migration and invasion in 786-O and 769 cells, assessed by transwell assays. G Knockdown of MAGI3 expression promotes lung metastasis in a ccRCC xenograft model. 786-O/shCtrl or 786-O/shMAGI3 cells were injected into SCID/NOD mice ( n = 15) via tail vein. The mice were sacrificed after 3 months, and the number of pulmonary metastatic nodules was statistically analyzed.

Article Snippet: Human renal cancer cell lines 769-P (CLS Cat# 300106/p490_769-P, RRID: CVCL_1050), 786-O (RRID: CVCL_1051), and 293T (DSMZ Cat# ACC-305, RRID: CVCL_0045) were obtained from ATCC.

Techniques: Expressing, Gene Expression, Biomarker Discovery, Over Expression, Knockdown, Western Blot, Migration, In Vitro, Wound Healing Assay, Injection

Journal: Cell Death & Disease

Article Title: MAGI3 deficiency unleashes β-catenin conformational change to drive metastatic progression and mTOR inhibitor resistance in ccRCC

doi: 10.1038/s41419-026-08563-x

Figure Lengend Snippet: A – C MAGI3 exhibits a negative correlation with β-catenin protein level and Wnt signaling activation in ccRCC specimens. Low MAGI3 level was associated with Wnt signaling activation in ccRCC, as evidenced by enriched gene signatures of Wnt/β-catenin activation in patients with lower MAGI3 levels in TCGA KIRC and GSE73731 datasets ( A ). MAGI3 does not correlate with β-catenin at mRNA levels in clinical specimens ( B ). MAGI3 negatively correlates with β-catenin at protein levels in THPA KIRC datasets ( C ). D , E Overexpression of MAGI3 reduces β-catenin protein level, while knockdown of MAGI3 increased β-catenin protein level in 786-O or 769-P cells. Cells stably transfected with MAGI3 or Ctrl ( D ), or knockdown with shMAGI3 or shCtrl constructs ( E ), were subjected to western blotting analysis to measure the levels of β-catenin, MAGI3 and β-actin protein. F , G Overexpression of MAGI3 decreased the half-lives of β-catenin protein via its interaction with MAGI3. 293T cells were transiently transfected with Flag-β-catenin-wt ( F ) or Flag-β-catenin-T779A ( G ) in absence or presence of GFP-MAGI3 respectively, were treated with CHX (25 μg/mL) for the indicated time before cell harvest for western blotting. Band density was quantified using ImageJ software. Data represent three independent experiments ( n = 3). * p < 0.05; ns, no significant difference ( t test). H Overexpression of MAGI3 promotes β-catenin ubiquitination. I The interaction with β-catenin is essential for MAGI3 to promote β-catenin ubiquitination. 293T cells were transiently transfected with Flag-β-catenin-wt or Flag-β-catenin-Δ773-781 in absence or presence of His-MAGI3 respectively, were treated with MG132 for 10 h. Cell lysates were subjected to IP with anti-Flag antibody-coupled beads. The precipitated complexes were probed with anti-ubiquitin antibody to detect ubiquitinated Flag-β-catenin.

Article Snippet: Human renal cancer cell lines 769-P (CLS Cat# 300106/p490_769-P, RRID: CVCL_1050), 786-O (RRID: CVCL_1051), and 293T (DSMZ Cat# ACC-305, RRID: CVCL_0045) were obtained from ATCC.

Techniques: Activation Assay, Over Expression, Knockdown, Stable Transfection, Transfection, Construct, Western Blot, Software, Ubiquitin Proteomics

Journal: Cell Death & Disease

Article Title: MAGI3 deficiency unleashes β-catenin conformational change to drive metastatic progression and mTOR inhibitor resistance in ccRCC

doi: 10.1038/s41419-026-08563-x

Figure Lengend Snippet: A , B Overexpression MAGI3 enhanced β-catenin phosphorylation and reduces β-catenin protein level in 786-O or 769-P cells. Knockdown MAGI3 reduces β-catenin phosphorylation and increases β-catenin protein level in 786-O or 769-P cells. Cell stably transfected with MAGI3 or Ctrl ( A ), or knockdown with shMAGI3 or shCtrl ( B ) constructs respectively, were subjected to western blotting analysis. Phosphorylation of β-catenin at Ser33/Ser37/Thr41 was detected with anti-phospho-β-catenin (Ser33/Ser37/Thr41) antibody. C MAGI3 serves as a scaffold protein to facilitate the interaction between GSK3β and β-catenin. D The C-terminus of β-catenin plays an indispensable role in MAGI3-mediated enhancement of the association between GSK3β and β-catenin. 293T cells were transiently transfected with Flag-β-catenin-wt or Flag-β-catenin-Δ773-781 (Flag-β-cat-Δ773-781) along with HA-GSK3β in presence or absence of His-MAGI3. Lysates were precipitated with an anti-Flag antibody and blotted with anti-His, anti-Flag or anti-HA antibody respectively. E Knockdown of MAGI3 inhibits the endogenous interaction between GSK3β and β-catenin, and suppresses the ubiquitination of β-catenin. Cell lysates were subjected to IP with anti-β-catenin antibody-coupled beads. The precipitated complexes were probed with anti-β-catenin, anti-ubiquitin and anti-GSK3β antibody to detect ubiquitinated β-catenin and its interaction with GSK3β. F Intramolecular interaction of β-catenin N-tail (β-cat-N-tail) with its ARM (β-cat-ARM) domain forms a loop structure. β-catenin GST fusion proteins containing the indicated domains were utilized to pull down cell lysates from 293T cells transfected with Flag-β-cat-N-tail, and the pull downed complexes were detected by western blotting. G MAGI3 significantly reduces the binding of extra molecular Flag-β-cat-N-tail with β-catenin. H The C-terminus of β-catenin was indispensable for MAGI3-mediated reduction in the interaction of extra molecular Flag-β-cat-N-tail with β-catenin. β-catenin GST fusion proteins containing the indicated domains were used to pull down cell lysates from 293T transfected with Flag-β-cat-N-tail with or without His-MAGI3, and the pull downed complexes were detected by western blotting.

Article Snippet: Human renal cancer cell lines 769-P (CLS Cat# 300106/p490_769-P, RRID: CVCL_1050), 786-O (RRID: CVCL_1051), and 293T (DSMZ Cat# ACC-305, RRID: CVCL_0045) were obtained from ATCC.

Techniques: Over Expression, Phospho-proteomics, Knockdown, Stable Transfection, Transfection, Construct, Western Blot, Ubiquitin Proteomics, Binding Assay

Journal: Cell Death & Disease

Article Title: MAGI3 deficiency unleashes β-catenin conformational change to drive metastatic progression and mTOR inhibitor resistance in ccRCC

doi: 10.1038/s41419-026-08563-x

Figure Lengend Snippet: A , B IHC analysis of MAGI3 and β-catenin expression in ccRCC specimens from 119 patients. Representative images of MAGI3 and β-catenin staining in patients with low and high MAGI3 expression levels. Scale bars: 200 μm. Magnified views of the wireframe regions are shown in the right panels. Scale bars: 50 μm. C , D Knockdown of β-catenin rescues the increased cell migration and invasion induced by MAGI3 knockdown. 786-O and 769-P cells were transfected with shMAGI3 alone, or in combination with β-catenin siRNA. Migration and invasion were assessed using transwell assays. E , F Blocking Wnt/β-catenin signaling rescues the increased cell migration and invasion induced by MAGI3 knockdown. 786-O and 769-P cells were transfected with shMAGI3 alone, or in combination with IWR-1-endo, an inhibitor of the Wnt/β-catenin pathway. Migration and invasion were assessed using transwell assays ( t test; * p < 0.05; ** p < 0.01; *** p < 0.001; ns, no significant difference; values represent mean ± SD, n = 3).

Article Snippet: Human renal cancer cell lines 769-P (CLS Cat# 300106/p490_769-P, RRID: CVCL_1050), 786-O (RRID: CVCL_1051), and 293T (DSMZ Cat# ACC-305, RRID: CVCL_0045) were obtained from ATCC.

Techniques: Expressing, Staining, Knockdown, Migration, Transfection, Blocking Assay

Journal: Cell Death & Disease

Article Title: MAGI3 deficiency unleashes β-catenin conformational change to drive metastatic progression and mTOR inhibitor resistance in ccRCC

doi: 10.1038/s41419-026-08563-x

Figure Lengend Snippet: A Knockdown of MAGI3 increased the IC 50 of Everolimus in 786-O and 769-P cells. Dose-response survival curves of MAGI3-knockdown 786-O and 769-P cells exposed to increasing concentrations of Everolimus for 48 h. Mean ± SD; n = 3; two-way ANOVA. B The reduced drug sensitivity caused by MAGI3 knockdown is restored by treatment with XAV-939, an inhibitor of the Wnt/β-catenin pathway. Cell viability of 786-O and 769-P cells was determined using CCK-8 assays. C , D MAGI3 knockdown promotes clonogenic formation in Everolimus-treated 786-O and 769-P cells, while concomitant treatment with XAV-939 and Everolimus markedly inhibits clonogenic formation. Colony formation assays were conducted in 786-O and 769-P cells treated with Everolimus in the absence or presence of XAV-939 for 14 days. Quantification analysis of clone formation assays. E Combination treatment with XAV939 and Everolimus synergistically inhibits cell invasion of ccRCC. Transwell invasion assays were conducted in 786-O and 769-P cells treated with Everolimus in the absence or presence of XAV-939 for 24 h. ( t test; * p < 0.05; ** p < 0.01; *** p < 0.001; ns, no significant difference; values represent mean ± SD, n = 3).

Article Snippet: Human renal cancer cell lines 769-P (CLS Cat# 300106/p490_769-P, RRID: CVCL_1050), 786-O (RRID: CVCL_1051), and 293T (DSMZ Cat# ACC-305, RRID: CVCL_0045) were obtained from ATCC.

Techniques: Knockdown, CCK-8 Assay

Journal: Biology Direct

Article Title: Acetylation- and ubiquitination-regulated SFMBT2 acts as a tumor suppressor in clear cell renal cell carcinoma

doi: 10.1186/s13062-024-00480-3

Figure Lengend Snippet: SFMBT2 knockdown facilitated proliferation and growth of clear cell RCC cells. A The cell ability was evaluated by MTT assay. B , C Plate colony formation assay was used to assess the colony formation capacity of 786-O and 769-P cells. D The cell percentage in phases. E The expression of cell cycle-related protein, cyclin E, cyclin D and p21 levels, was determined by western blot. F The 786-O cells with decreased expression of SFMBT2 were inoculated into nude mice, and the subcutaneous tumors were shown (the scale bar presented as 1 cm). G The tumor weight. H The tumor growth curve. I Immunohistochemistry staining was performed to determine the expression of SFMBT2 and Ki-67 in the tumors (the scale bar presented as 50 μm). * p < 0.05; ** p < 0.01; *** p < 0.001 versus LV-shNC

Article Snippet: Human renal cell carcinoma cell lines, 786-O and 769-P, were purchased from iCell (Shanghai, China), and culture with RPMI-1640 (Solarbio, Beijing, China) supplemented with 10% fetal bovine serum (FBS) (TIANHANG, Huzhou, Zhejiang, China) in a humid incubator with 37 °C and 5% CO 2 .

Techniques: MTT Assay, Colony Assay, Expressing, Western Blot, Immunohistochemistry, Staining

Journal: Biology Direct

Article Title: Acetylation- and ubiquitination-regulated SFMBT2 acts as a tumor suppressor in clear cell renal cell carcinoma

doi: 10.1186/s13062-024-00480-3

Figure Lengend Snippet: Silencing of SFMBT2 promoted the migration, invasion and metastasis of clear cell RCC cells. A , B The migratory ability of 786-O and 769-P cells was evaluated by wound healing assay (the scale bar presented 200 μm). C , D The invasion of cells were assessed by transwell assay with matrigel supplementary (the scale bar presented 100 μm). E The GFP-stably-expressed 786-O cells were intravenously injected into nude mice, and the in vivo bioluminescence imaging was done. F , G The lung was isolated from mice, and the nodule numbers in lung were counted. H The pathological features of lung from 786-O cell-inoculated mice were detected by HE staining (the scale bar presented 50 μm). * p < 0.05; ** p < 0.01; *** p < 0.001 versus LV-shNC

Article Snippet: Human renal cell carcinoma cell lines, 786-O and 769-P, were purchased from iCell (Shanghai, China), and culture with RPMI-1640 (Solarbio, Beijing, China) supplemented with 10% fetal bovine serum (FBS) (TIANHANG, Huzhou, Zhejiang, China) in a humid incubator with 37 °C and 5% CO 2 .

Techniques: Migration, Wound Healing Assay, Transwell Assay, Stable Transfection, Injection, In Vivo, Imaging, Isolation, Staining

Journal: Oncology Reports

Article Title: Downregulation of microRNA-15a suppresses the proliferation and invasion of renal cell carcinoma via direct targeting of eIF4E

doi: 10.3892/or.2017.5901

Figure Lengend Snippet: Expression of miR-15a is downregulated in RCC tissues and cell lines. (A) qRT-PCR detection of miR-15a expression in 40 RCC specimens and adjacent normal tissues. (B) qRT-PCR detection of miR-15a expression in 4 RCC cell lines and normal renal cell line HK-2. (C) Correlation between miR-15a and eIF4E mRNA in RCC tissues using linear correlation. Each experiment was repeated at least 3 times; *P<0.05, **P<0.01 vs. the control group.

Article Snippet: The human renal carcinoma cell lines (ACHN, 786-O, 769-P and OS-RC-2) and normal renal cell line HK-2 were obtained from the China Center for Type Culture Collection (CCTCC; Shanghai, China).

Techniques: Expressing, Quantitative RT-PCR, Control