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Transcriptomic data of Bevacizumab-adapted colorectal adenocarcinoma cells HCT116

ABSTRACT: Transcriptomic data of Bevacizumab-adapted colorectal adenocarcinoma cells HCT116

PROVIDER: PRJNA916900 | ENA |

REPOSITORIES: ENA

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Transcriptomic data of Bevacizumab-adapted colorectal adenocarcinoma cells HCT116

Project description:Determination of the ion channel and transporters gene expression profile of Bevacizumab-adapted colorectal adenocarcinoma cells HCT116

2023-01-02 | GSE221948 | GEO

TAS-102, Irinotecan, and Bevacizumab in Pre-treated Metastatic Colorectal Cancer (TABAsCO), A Phase II Clinical Trial. ClinicalTrials.gov NCT04109924

Project description:Background: The efficacy of FOLFIRI plus an antiangiogenesis biologic agent as 2nd line therapy for metastatic colorectal adenocarcinoma is limited. TAS-102 is a novel oral antimetabolite with a distinct mechanism of action from fluoropyrimidines. We evaluated the antitumor efficacy of TAS-102, irinotecan and bevacizumab in patients with pre-treated, advanced colorectal adenocarcinoma in a multicenter, phase II, single-arm study. Methods: Patients with advanced colorectal adenocarcinoma who had progressed after oxaliplatin and fluoropyrimidine and were eligible for treatment with bevacizumab were treated with irinotecan, bevacizumab, and TAS-102 in 28-day cycles. The primary endpoint was progression-free survival (PFS). Results: We enrolled 35 evaluable patients. The study was positive. The median PFS was 7.9 (90% CI 6.2-11.8) months (vs. 6 months in historical control, p=0.018). The median overall survival was 16.5 (90% CI 9.8-17.5) months. Sixty-seven percent of patients experienced grade 3 or higher treatment-related adverse events. The most common toxicities were hematological (neutropenia) and gastrointestinal (diarrhea, nausea, and vomiting). Conclusions: Irinotecan, TAS-102 and bevacizumab is an active 2nd line therapy for patients with metastatic colorectal adenocarcinoma. Neutropenia is common and can affect dose density/intensity mandating use of G-CSF. A randomized study versus standard of care therapy is warranted.

2024-08-26 | GSE275628 | GEO

Mucinous colorectal adenocarcinoma

Project description:Mucinous colorectal adenocarcinoma

| PRJNA992109 | ENA

RNA-Seq of SMG1-SMG8-SMG9 complex alterations in human colorectal adenocarcinoma cell line HCT116

Project description:Nonsense-mediated mRNA decay (NMD) is a translation-dependent mRNA turnover pathway, which degrades transcripts containing premature termination codons. The execution of NMD requires the phosphorylation of N- and C-terminal tails of the key NMD factor UPF1, which thereby serve as binding platforms for the degradation factors SMG5, SMG6 and SMG7. UPF1 phosphorylation is mediated by the kinase SMG1, whose activity is regulated by a heterodimer consisting of SMG8 and SMG9. Recent work indicated that SMG9 functions as a bridge between SMG1 and SMG8, allowing the C-terminus of SMG8 to elicits its role of stabilizing the autoinhibitory state of SMG1. Here, we deleted the C-terminus of endogenous SMG8 in human colorectal adenocarcinoma cell line HCT116 via CRISPR-Cas9. In addition, we established SMG8- and SMG9-depleted cells. With these cell lines we wanted to explore the regulatory role of SMG8 and SMG9 for NMD execution. Furthermore, we tested the transcriptomic changes upon treatment of cells with the SMG1 inhibitor SMG1i, which functions as an ATP-competitive inhibitor and binds to the active site of SMG1. Cells were treated with 0, 0.1 or 1 μM SMG1i for 24 h. As controls, the HCT116 wildtype cells were treated with DMSO.

2026-02-13 | E-MTAB-13949 | biostudies-arrayexpress

Prediction of response to bevacizumab

Project description:The patients who underwent surgery for primary lesions were examined. All patients had metastatic or recurrent CRC and received bevacizumab therapy as first line or second line treatment. Responders and nonresponders were determined based on RECIST and confirmed by CT or MRI. Gene-expression profiles of primary CRC were determined using Human Genome GeneChip arrays U133. Colorectal cancer patients who had undergone surgical resection of colorectal cancer were studied. To identify molecular signatures to predict response to bevacizumab, gene expression profiles were compared between Reponder and Non-responder.

2013-01-03 | E-GEOD-19862 | biostudies-arrayexpress

Transcriptomic data of bevacizumab-adapted colorectal adenocarcinoma cells HCT-116.

Project description: Not available

| S-EPMC10090242 | biostudies-literature

PKM2 lactylation promotes colorectal cancer vasculogenic mimicry and resistance to bevacizumab treatment by facilitating FOSL1 super-enhancer formation [CUT&Tag]

Project description:Despite the clinical utility of bevacizumab in advanced colorectal cancer (CRC), resistance remains a major challenge. Here, we unveiled a lactate-mediated mechanism driving vasculogenic mimicry (VM) and bevacizumab resistance through PKM2 lactylation. PKM2 lactylation at K206 by AARS1 promoted PKM2 nuclear translocation and interaction with FOSL1. PKM2 binding facilitated FOSL1-dependent super-enhancer formation and target gene transcription, which contributed to CRC cell VM. Genetic or pharmacological inhibition of PKM2 lactylation disrupted VM and synergized with bevacizumab in patient-derived pre-clinical models, significantly improving therapeutic efficacy. Together, this study reveals lactylation as a metabolic switch linking cancer glycolytic reprogramming to transcriptional rewiring and proposes targeting PKM2 lactylation to enhance the anti-tumor activity of bevacizumab in CRC.

2026-02-14 | GSE307936 | GEO

PKM2 lactylation promotes colorectal cancer vasculogenic mimicry and resistance to bevacizumab treatment by facilitating FOSL1 super-enhancer formation [ATAC-seq]

2026-02-14 | GSE307935 | GEO

PKM2 lactylation promotes colorectal cancer vasculogenic mimicry and resistance to bevacizumab treatment by facilitating FOSL1 super-enhancer formation [RNA-Seq]

2026-02-14 | GSE307937 | GEO

hPTTG1-/- HCT116 human colorectal cancer cells: pcDNA3.1 control vs. pcDNA3.1-hPTTG1

Project description:Transcriptional profiling of hPTTG1-/- HCT116 human colorectal cancer cells comparing hPTTG1-/- HCT116 cells transfected with pcDNA3.1, and with hPTTG1-/- HCT116 cells transfected with pcDNA3.1-hPTTG1 plasmid.

2014-01-02 | GSE26434 | GEO

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