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Chidamide combined with cytarabine plays a role in the treatment of AML by down-regulating the MYC-RRP9 pathway

ABSTRACT: Chidamide combined with cytarabine plays a role in the treatment of AML by down-regulating the MYC-RRP9 pathway

PROVIDER: PRJNA970231 | ENA |

REPOSITORIES: ENA

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Chidamide combined with cytarabine plays a role in the treatment of AML by down-regulating the MYC-RRP9 pathway

Project description:To provide a new treatment strategy for patients with acute myeloid leukemia (AML), we investigated the therapeutic effect and mechanism of chidamide combined with cytarabine in AML.

2023-05-12 | GSE231914 | GEO

Transcriptional profile of AML xenografts treated with either PBS or a combination of decitabine and cytarabine

Project description:The Affymetrix Human Genome U133 Plus 2.0 Array was used to examine the Genome wide transcriptional changes which follow the treatment of AML xenografts with either PBS control or combination of decitabine (DAC) and cytarabine (Ara-C). Animals were treated with PBS, DAC alone, Ara-C alone, DAC and Ara-C combined (D+A), DAC followed by Ara-C (D/A) or Ara-C followed by DAC (A/D). PBS vs each drug combination

2013-03-06 | E-GEOD-44857 | biostudies-arrayexpress

Posttranslational splicing modifications as a key mechanism in cytarabine resistance in AML

Project description:Despite the approval of several drugs for AML, cytarabine is still widely used as a therapeutic approach. However, most patients show resistance and only 10% of them overcome the disease. Using high-throughput screening analysis, we show that phosphorylation levels of SR proteins were elevated during cytarabine resistance. Moreover, phosphorylation of SR proteins at diagnosis was different between responder and non-responder patients, pointing to their utility to predict response. These changes correlated with altered transcriptomic profiles of SR protein target genes.

2023-07-04 | PXD034010 | Pride

Chidamide inhibits double expressor lymphoma through repressing Myc expression and activity

Project description:Double-expressor lymphoma (DEL), defined by MYC and BCL-2 overexpression without corresponding chromosome translocations, is often associated with poor outcomes for standard treatment (R-CHOP). Recently, inhibitors of histone deacetylases have shown great effect in T cell lymphomas. However, its effects on B cell lymphomas are mild. Here, our clinical retrospective analysis showed that HDAC inhibitor chidamide combined with R-CHOP (CR-CHOP) can dramatically increase the complete remission rate of patients with DEL. And the sensitivity of B cell lymphoma cell lines to chidamide is negatively correlated to Myc level. From Western blots and transcriptomics analysis, we found that chidamide treatment could reduce Myc protein level and downregulate the transcription levels of corresponding Myc downstream targets. Thus our results indicate that HDAC inhibitor chidamde holds great potential for treating DEL, which likely functions through inhibiting the Myc pathway.

2022-04-24 | GSE173285 | GEO

Transcriptional profile of AML xenografts treated with either PBS or a combination of decitabine and cytarabine

2013-03-06 | GSE44857 | GEO

Chidamide suppresses adipogenic differentiation of bone marrow derived mesenchymal stem cells

Project description:To explore the potential mechanism of chidamide in BM-MSC-mediated adipogenesis, we have employed mRNA microarray expression profiling platform to identify significant differential genes associated with adipogenic differentiation and chidamide management.

2022-04-13 | GSE199466 | GEO

Chidamide inhibits the NOTCH1-MYC signaling axis in T-cell acute lymphoblastic leukemia

Project description:We report that Chidamide shows significant anti- proliferation and more specifically anti-NOTCH effects in both cell lines and primary cells of T-ALL patients. By analyzing the expression profile characterizing the response of the cell lines to Chidamide treatment, we further confirmed that the antitumor effect of Chidamide was due to the inhibition of HDAC and the anti-NOTCH1 effect.

2021-12-31 | GSE160349 | GEO

Chidamide effect on MM

Project description:Chidamide effect on MM

| PRJNA658123 | ENA

CREBBP cooperates with cell cycle machinery to attenuate chidamide sensitivity in relapsed/refractory DLBCL

Project description:Frequent inactivating mutations of histone acetyltransferase CREBBP is a characteristic feature of diffuse large B-cell lymphoma (DLBCL), highlighting the attractiveness of targeting the CREBBP deficiency as a therapeutic strategy. In this study, we demonstrate that chidamide, a novel histone deacetylase (HDAC) inhibitor, is effective in treating a subgroup of relapsed/refractory DLBCL patients, achieving an overall response rate (ORR) of 25.0% and a complete response (CR) rate of 15.0%. However, the clinical response to chidamide remains poor as most patients exhibit resistance, hampering the clinical utility of the drug. Functional studies in both in vitro and in vivo models showed that CREBBP loss of function is correlated with chidamide sensitivity, which is associated with modulating cell cycle machinery. A combinatorial drug screening of 130 kinase inhibitors targeting cell cycle regulators identified AURKA inhibitors, which inhibited G2/M transition during cell cycling, as top candidates that synergistically enhanced antitumor effects of chidamide in CREBBP-proficient DLBCL cells. Our study demonstrated that CREBBP inactivation can serve as a potential biomarker to predict chidamide sensitivity, while a combination of AURKA inhibitor and chidamide provides a novel therapeutic strategy for the treatment of relapsed/refractory DLBCL.

2024-02-24 | GSE167383 | GEO

Chidamide triggers BTG1-mediated autophagy and reverses the chemotherapy resistance in the relapsed/refractory B cell lymphoma

Project description:Rituximab/chemotherapy relapsed and refractory B cell lymphoma patients have a poor overall prognosis, and it is urgent to develop novel drugs for improving the therapies of these patients. A new oral histone deacetylase inhibitor, chidamide shows anti-tumor activity by activating the pro-apoptosis pathway in some other hematological malignancies, suggesting its potential application to the relapsed and refractory B cell lymphoma. In this study, we examined the therapeutic effects of chidamide on the cell and mouse models of the rituximab/chemotherapy resistant B cell lymphoma, as well as the primary B cell lymphoma cells. In Raji-4RH and RL-4RH cells, the rituximab/chemotherapy resistant B cell lymphoma cell lines (RRCL), chidamide treatment induced growth inhibition and G0/G1 cell cycle arrest, which were associated with E2F1/2 inactivation and CDK2 degradation. The primary B cell lymphoma cells from Rituximab/chemotherapy relapsed and refractory patients were also very sensitive to chidamide treatment. Interestingly, chidamide triggered the cell death via the autophagy pathway instead of the activation of apoptosis in Raji-4RH and RL-4RH cells, likely due to the lack of the pro-apoptotic proteins in these resistant cells. In the RNA-seq and chromatin immunoprecipitation (ChIP) analysis, we identified BTG1 and FOXO1 as the direct target genes of chidamide, which control the autophagy and cell cycle respectively in RRCL treated with chidamide. Moreover, the combination of chidamide with the chemotherapy drug Cisplatin sensitized the RRCL to growth inhibition in a synergistic manner. Chidamide-Cisplatin combination significantly reduced the tumor burden of a mouse lymphoma model established with engraftment of RRCL. Taken together, our studies provides a theoretic and mechanistic basis for further evaluation of the chidamide-based clinical trial for rituximab/chemotherapy relapsed and refractory B cell lymphoma patients.

2021-10-06 | GSE137359 | GEO

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