PMCID string | Title string | Sentences string |
|---|---|---|
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | For instance, imatinib, as a first‐line therapy, has significantly improved GIST patient survival . |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | However, most patients eventually experience disease progression due to KIT secondary mutations, including activation loop and gatekeeper mutations . |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | Although regorafenib, sunitinib and ripretinib have been approved to overcome imatinib‐resistant mutations of KIT, they both show toxicity and poor clinical responses . |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | Several new KIT inhibitors against imatinib‐resistant secondary mutations are currently being evaluated in clinical trials, such as pazopanib , anlotinib and dovitinib . |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | In addition, many candidate KIT inhibitors are in preclinical development, such as CHMFL‐KIT‐033/8140 and AZD3229 . |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | However, it takes a long time to complete clinical research, and these drugs are temporarily unable to fulfil the urgent clinical demand. |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | It has been demonstrated that imatinib resistance in GISTs is caused by the feedback activation of FGF signalling, which results in a rebound in ERK phosphorylation . |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | The combination of the pan‐FGFR inhibitors BGJ398 and imatinib repressed ERK rebound and enhanced the antitumour activity of imatinib in GISTs. |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | In addition, the Memorial Sloan Kettering Cancer Center (MSKCC) conducted a phase I clinical trial with a combination of imatinib and BGJ398 (Trial Registration: NCT02257541) for patients with locally advanced or metastatic GISTs. |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | Approximately 30% of the evaluable study cohort attained durable stabilization of disease lasting at least 32 weeks. |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | However, combination toxicity was an important factor that limited the ability of this study to meet its primary end point . |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | Therefore, there remains an urgent need for more agents that can inhibit both the different resistance mutations of KIT and FGFRs, which are usually highly expressed in GISTs and participate signalling crosstalk with KIT, causing imatinib resistance . |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | In this study, through high‐throughput screening using a functional isogenic BaF3 cell library, we found that nintedanib, a triple angiokinase inhibitor of FGFR/VEGFR/PDGFR that has been approved for the treatment of IPF and NSCLC, exhibited potent activity against a panel of primary gain‐of‐function (GOF) mutations and secondary drug resistance mutations in KIT kinase. |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | Interestingly, in addition to better efficacy against KIT wt, nintedanib showed potent inhibitory effects against primary GOF mutations (V559A/D/G and L576P), a few secondary imatinib‐resistant mutations in the ATP binding pocket (such as V654A and T670I) and activation loops (such as D820E/G/Y, D816E/H/V, A829P) and sunitinib‐resistant mutations such as D816H/V and A829P). |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | Because nintedanib is a multi‐targeted kinase inhibitor, we believe that this antitumour activity is not only contributed by KIT inhibition alone, its inhibition on other kinases, such as VEGFR and PDGFR, may also play a role. |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | However, nintedanib could not completely overcome the resistance mediated by MAP kinase activation via FGF signalling, which may be due to the low drug concentration in tumours or the weak inhibition of FGFR by nintedanib. |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | In summary, nintedanib eliminated the adaptive response after KIT inhibition in imatinib‐sensitive GISTs. |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | Additionally, nintedanib may be effective in the imatinib‐resistant clones containing acquired mutations in KIT kinase and FGFR feedback activation that have emerged. |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | The findings described here support a basis for extending the application of nintedanib as a new strategy to improve the treatment of GIST patients with de novo or acquired resistance to imatinib. |
PMC9019892 | Nintedanib overcomes drug resistance from upregulation of FGFR signalling and imatinib‐induced KIT mutations in gastrointestinal stromal tumours | The peer review history for this article is available at https://publons.com/publon/10.1002/1878‐0261.13199. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The most commonly occurring sarcoma of the soft tissue is gastrointestinal stromal tumor (GIST). |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Treatment and prevention of the disease necessitate an understanding of the molecular mechanisms involved. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | However, the role of BRD4 in the progression of GIST is still unclear. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | While it is known there are abundant infiltrating tumor-associated macrophages (TAMs) in the tumor microenvironment, the exact role of these cells has yet to be studied. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | This work showed an upregulation of BRD4 in GIST that was associated with GIST prognosis. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Through gain and loss of function studies, it was found that BRD4 promotes GIST growth and angiogenesis in vitro and in vivo. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Mechanistically, BRD4 enhances CCL2 expression by activating the NF-κB signaling pathway. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Furthermore, this CCL2 upregulation causes recruitment of macrophages into the tumor leading to tumor growth. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | A likely mechanism for interactions in the GIST microenvironment has been outlined by this work to show the role and potential use of BRD4 as a treatment target in GIST.Among sarcomas of soft tissue, the most ubiquitous cancer is gastrointestinal stromal tumor (GIST) with gastrointestinal tract localization. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Previous research suggests the role of KIT and PDGFRA oncogenic mutations in interstitial cells of Cajal, which are mesenchymal pacemaker cells, in disease metastasis, proliferation, and tumorigenesis. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | These mutations in GIST are targeted by molecular drugs, such as imatinib. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Despite the use of such specific drugs that alter the treatment scenario, resistance leads to recurrence in a substantial number of patients. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Another challenge is a lack of effective therapy for GIST when the abovementioned genes are not mutated. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | These shortcoming call for the analysis of the disease mechanisms to consider new therapeutic approaches. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | There are various cells that are not malignant in the tumor microenvironment, such as the most aboundant tumor-associated macrophages (TAMs), which are ubiquitous hematopoietic cells with a migratory nature. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | There are many clinical and epidemiological studies that have highlighted the poor cancer prognosis related to GIST and the number of TAMs. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The progression of cancer involves discrete signals of the microenvironment that influence different cells, such as macrophages. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The tumor microenvironment that influences macrophage orientation and differentiation is influenced by the profile of chemokines at the tumor site. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | An example is the upregulation and role of chemokine (C–C motif) ligand 2 (CCL2) in many cancers, including GIST. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Bromodomain proteins include the mammalian bromodomain and extraterminal domain (BET) family inclusive of BRD2, 3, and 4. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Research has focused on the functioning of BRD2 and 4 in elongation during transcription and regulation of the cell cycle while their possible involvement in inflammation is yet to be uncovered. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | BRD4 has recently been shown to regulate RNA polymerase II elongation and the expression of genes involved in NF-κB-associated inflammation via activation of P-TEFb complex by CDK9. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | In the current study, we identified BRD4, which was markedly upregulated and showed a significant association with pathology and survival in GIST patients. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The expression of CCL2 was increased by BRD4 overexpression via the NF-κB signaling pathway, which led to TAM recruitment, ultimately contributing to tumor growth. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | These findings suggest that BRD4 is involved in GIST via TAMs. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Jonathan Fletcher (DanaFarber Cancer Institute, Boston, MA) kindly provided the GIST882 cell line (from a patient with a K642E: KIT exon 13 homozygous missense mutation). |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Biowit Technologies (Shenzhen, China) was the source of the procured GIST-T1 cell line (from a patient with a V560Y579del: 57 nucleotide inframe mutation in KIT exon 11). |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Dulbecco’s Modified Eagle Medium (DMEM) plus 10% fetal bovine serum (FBS) and 1% penicillin–streptomycin were used for culturing at 5% CO2 at 37 °C. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Patients (with written informed consent) who went through surgery at the Second Hospital of Jilin University in the period from February 2012 to March 2015 were the source of the 20 GIST samples used in this study; samples were fixed in formalin and embedded in paraffin. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The samples were subjected to snap freezing in liquid nitrogen and stored at −80 °C untill assayed. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | HE staining was used by two pathologists to pathologically confirm the samples. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The Committees for Ethical Review of Research Involving Human Subjects at the Second Hospital of Jilin University issued an approval for ethical consent. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Sectioning of the samples fixed in formalin and embedded in paraffin into 4-μm sections was performed. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Individually, BRD4, CD31, and CD68 antibody staining was performed with selected slides that were then analyzed by two experienced pathologists. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | After normalization to the staining of the nucleus and the cytoplasm, the staining intensity scores were based on the following scoring system: 0 = no staining; 1 = weak staining; 2 = moderate staining; and 3 = strong staining. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The combination of these scores with the positive cell percentage yielded the final immunohistochemistry (IHC) score. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Quantitative real-time PCR (qRT-PCR) was performed as previously described. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Briefly, TRIzol Reagent (Invitrogen) was used to extract total RNA, followed by reverse transcription with SuperScript II Reverse Transcriptase (Invitrogen) in accordance with the protocols of the manufacturer. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | An ABI 7300 real-time PCR system (Applied Biosystems) was used for the analysis with primers specific for BRD4 and GAPDH. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The 2 method was employed for assessing the changes in the expression of BRD4, with the control being GAPDH mRNA levels. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Western blotting was performed as previously described. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | RIPA buffer (Pierce, Rockford, IL, USA) plus a protease inhibitor cocktail (Roche, Pleasanton, CA, USA) was utilized for lysing cells. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Sodium dodecyl sulfate–polyacrylamide gel electrophoresis was utilized for resolving proteins, followed by the transfer of proteins to polyvinylidene difluoride membranes. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Overnight incubation with primary antibodies was performed at 4 °C, followed by exposure to the corresponding secondary antibodies conjugated to horseradish peroxidase (HRP). |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Then, blots were incubated with the corresponding HRP-conjugated secondary antibodies. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | ECL regents (Thermo Scientific) were used to observe the resulting bands. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The antibodies used in this study were as follows: BRD4 (ab128874), β-actin (ab8226), MMP9 (ab38898), LOX (ab174316), VEGFA (ab52917), p65 (ab16502), p-p65 (ab86299), Lamin A/C (ab108595), and CCL2 (ab9851; Abcam). |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Cells were seeded into 96-well plates, followed by an exchange of the media to one with CCK8 (100 μl for 10 μl of the latter) for 1 h after overnight culture. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The optical density (OD) was measured using absorbance at 450 nm at various time points: 24, 48, and 72 h. This protocol was in accordance with that used in a previous study. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | To summarize, six-well plates were used for overnight culture of cells, and cells were subsequently incubated with 10 μg/ml BrdU for 20 min. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | This was followed by a double phosphate-buffered saline (PBS) wash and overnight fixation utilizing 70% ethanol at −20 °C. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | This was followed by a 45 min denaturation in 2 N HCL and FITC secondary antibody staining at room temperature for 1 h. Then, 40 g/ml RNase A and 200 g/ml PI were added for 30 min, followed by flow cytometry analysis. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The Buffy coats from healthy voluteers were used to isolate human monocytes. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Ficoll-Hypaque (Pharmacia Corporation) was utilized to isolate peripheral blood monocytes followed by density gradient centrifugation for 50 min at 400 g. Cells were seeded into 24-well plates at a density of 2 × 10 cells/ml in RPMI 1640 medium plus 10% heat-inactivated human AB serum, 50 U penicillin and streptomycin/ml, 2 mM L-glutamine, and 100 ng/ml human macrophage colony-stimulating factor, which was aimed at stimulating the differentiation of macrophages. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Warm medium was used to wash away the cells that did not adhere gently and repeatedly after 6 days of culture. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | CD14 macrophages constituted over 95% of the adherent cells using this approach. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | For the activation of M1 macrophages in vitro, 2 × 10 cells/l of the isolated cells (as described above) were treated for 1 day with 25 μg/ml LPS (lipopolysaccharide; Sigma) to the above-isolated cells, while for the activation of M2-polarized macrophages, 45 ng/ml recombinant human interleukin-4 (IL-4, R&D) was used. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Flow cytometry was conducted to check the differentiated macrophages from monocytes. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Conditioned media for the next round of in vitro experiments was obtained from PBS washing of cells followed by incubation in medium minus supplements for another 24 h. Endothelial cell tube formation was performed as previously described. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Incubation of the GIST cell lines in DMEM minus serum was done as indicated overnight. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Ninety-six-well plates with Matrigel were seeded with 20,000 HUVECs per well along with the above-described conditioned medium. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | After incubation, imaging of tube formation by microscopy and quantification the branch number in the formed HUVEC tubes were performed. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | After treatment in DMEM minus serum overnight as indicated, conditioned medium was collected from the cells for VEGFA-enzyme-linked immunosorbent assay (ELISA) analysis in accordance with the prescribed protocols of the manufacturer. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The absorbance at 470 nm was recorded for the OD values. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The assay for wound healing involved six-well plates used for seeding GIST cells. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | A sterile 200-μm plastic pipette tip was employed to softly scratch the monolayer once cells were 95% confluent, followed by documentation of the wound with photographs. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The Transwell invasion assay involved seeding of 4 × 10 cells suspended in medium lacking serum in the membranes of the upper chamber without/with Matrigel (BD Biosciences) coating. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The lower chamber received 600 μl medium plus 10% FBS. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | After 24 h, the membrane bottom was subjected to 30-min fixation and 0.1% crystal violet staining. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Following the use of a cotton swab to wipe the interior of the membrane, microscopy was utilized to quantify the cells. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Six-well plates were used to culture 500–1000 cells/well that has been exposed to the aforementioned chemicals and combinations. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Renewal of the medium was performed every third day untill the 14th day, after which cells were fixed and stained with crystal violet. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Cells that had been exposed to drugs were compared to control cells exposed to DMSO, and assays were completed in triplicate. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The Animal Care and Use Committee of the Second Hospital of Jilin University issued approval for the following experiments. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Balb/c nude mice (famale, 4 weeks in age) were randomly divided into two groups (n = 6). |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The animals received subcutaneous administration of GIST-882 cells that expressed the vector or BRD4 resuspended in PBS with Matrigel (1:1). |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The tumor volumes were computed with the following formula expression once a visible tumor mass had developed in the animals: (length × width)/2. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Animals were sacrificed 19 days after injection. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | Prism 5.0 (GraphPad software) was employed for analyses. |
PMC6901583 | RETRACTED ARTICLE: BRD4 promotes tumor progression and NF-κB/CCL2-dependent tumor-associated macrophage recruitment in GIST | The mean±s.d. |
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