Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chidamide and Anlotinib Synergistically Inhibit High Grade B-Cell Lymphomas via PI3K/AKT Signaling Pathway

ABSTRACT: Chidamide and Anlotinib Synergistically Inhibit High Grade B-Cell Lymphomas via PI3K/AKT Signaling Pathway

PROVIDER: PRJNA1237746 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR32754312_1.fastq.gz	Fastqsanger.gz
	SRR32754312_2.fastq.gz	Fastqsanger.gz
	SRR32754313_1.fastq.gz	Fastqsanger.gz
	SRR32754313_2.fastq.gz	Fastqsanger.gz
	SRR32754314_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Chidamide and Anlotinib Synergistically Inhibit High Grade B-Cell Lymphomas via PI3K/AKT Signaling Pathway

Project description:High-grade B-cell lymphoma with concurrent MYC and BCL2/BCL6 rearrangements (HGBL-DHL) presents a formidable challenge, often refractory and resistant to front-line immunochemotherapies, necessitating urgent exploration of novel therapeutic approaches. Herein, we unveiled a robust synergistic anti-lymphoma efficacy of chidamide and anlotinib against HGBL-DHL. The cooperative effect of cell proliferation inhibition, apoptosis induction, and cell cycle arrest were demonstrated in cell lines through Cell Counting Kit-8, and Annexin V/PI staining, respectively. Moreover, in an HGBL-DHL-xenografted mouse model, the combination therapy markedly reduced tumor burden without inducing fatal toxicity. Mechanistically, chidamide suppressed HDAC3, while anlotinib inhibited VEGFR2, leading to down-regulation of the PI3K/AKT signaling cascade. This dual suppression was by their synergistic effect. Collectively, our preclinical findings underscored the synergistic activity of chidamide and anlotinib combination against HGBL-DHL, warranting further clinical evaluation of this regimen for treating this challenging entity.

2025-05-17 | GSE292250 | GEO

Chidamide and Anlotinib act synergistically in Jurkat cells by inhibiting the Hippo signaling pathway

Project description:T-cell Acute Lymphoblastic Leukemia (T-ALL) is an aggressive hematologic malignancy characterized by drug resistance, relapse and poor prognosis. Chidamide, a histone deacetylase inhibitor, has shown epigenetic therapeutic potential in T-ALL, but its efficacy is limited and acquired drug resistance exists. To overcome these limitations, we systematically evaluated the synergistic Combination effects of three drug candidates, OTX-015 (BET inhibitor), Metformin (metabolic regulator), and Anlotinib (multitargeted tyrosine kinase inhibitor), with Chidamide.

2025-11-24 | GSE310869 | GEO

Chidamide and Anlotinib act synergistically in Jurkat cells by inhibiting the Hippo signaling pathway

Project description:Chidamide and Anlotinib act synergistically in Jurkat cells by inhibiting the Hippo signaling pathway

| PRJNA1367378 | ENA

Transcriptome profiling of Anlotinib-resistant NCI-H1975 and Anlotinib-treated Anlotinib-resistant NCI-H1975

Project description:Further to our previous study (E-MTAB-5997), here we performed transcriptome profiling on Anlotinib-resistant NCI-H1975 and Anlotinib-treated Anlotinib-resistant NCI-H1975, and would like to understand the effects of Anlotinib on Anlotinib-resistant NCI-H1975 cell, compare the different transcriptome profiling on NCI-H1975 cells and Anlotinib-resistant NCI-H1975 cells, sought to find the biomarker for explaining Anlotinib resistance.

2019-07-01 | E-MTAB-7068 | biostudies-arrayexpress

Dual Epigenetic and Nuclear Export Inhibition by Chidamide and Selinexor in High Grade B-Cell Lymphomas via Survivin and PI3K/AKT Inhibition

Project description:Double hit lymphoma (DHL) is a highly aggressive disease thatis resistant to conventional first-line immunochemotherapeutic regimens. This resistance necessitates the exploration of innovative therapeutic strategies. In this study, the combination of chidamide and selinexor showed significant synergistic antilymphoma effects in the treatment of DHL. The synergistic effects were evidenced by the inhibition of cell proliferation, induction of apoptosis, and perturbation of the cell cycle in cell lines, as assessed by Cell Counting Kit-8, Annexin V/PI staining, and PI staining assays. Furthermore, in a xenograft mouse model of DHL, this combination therapy markedly reduced the tumor burden without causing lethal toxicity. At the mechanistic level, the combination of chidamide and selinexor resulted in the synergistic downregulation of survivin and the PI3K/AKT signaling pathway. This dual inhibition was attributed to the interactive effects of the two drugs. The downregulation of key downstream targets of the PI3K/AKT pathway, including c-Myc, MCL1, BCL-XL, cyclin A2, and survivin, was synergistic and aligned with the phenotypic outcomes. Notably, survivin, an antiapoptotic protein and a direct target of HDAC3 and XPO1, was synergistically downregulated at the nuclear, cytoplasmic, and total protein levels by the combination of chidamide and selinexor, thereby inducing apoptosis. Our preclinical data highlighted the potential synergistic efficacy of chidamide and selinexor in targeting DHL, providing a rationale for further clinical investigation of this therapeutic combination for the treatment of this refractory disease.

2025-12-15 | GSE298302 | GEO

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

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

Transcriptome profiling of Anlotinib-resistant NCI-H1975 and Anlotinib-treated Anlotinib-resistant NCI-H1975

Project description:Transcriptome profiling of Anlotinib-resistant NCI-H1975 and Anlotinib-treated Anlotinib-resistant NCI-H1975

| PRJEB27916 | ENA

Role of Anlotinib-induced CCL2 decrease in anti-angiogensis and response prediction for Non-Small Cell Lung Cancer therapy

Project description:Purpose: Our previous clinical trials have been demonstrated that Anlotinib can inhibit tumor growth upon refractory advanced non-small cell lung cancer (NSCLC) patients with the possibility mechanism of anti-angiogenesis. The present study sought to reveal the underlying molecular mechanism of Anlotinib-induced anti-angiogenesis in advanced NSCLC. Experimental Design: Computed tomography (CT) was used to evaluate the treatment effect of Anlotinib upon refractory advanced NSCLC patients. Transcriptome profiling was performed to identify the key gene expression alteration in NCI-H1975 cells before and after Anlotinib treatment. NCI-H1975 derived xenograft model was applied to investigate treatment effect and verify anti-angiogenesis mechanism of Anlotinib. Results: Anlotinib induces tumor cytotoxicity on refractory advanced NSCLC patients, NCI-H1975 derived xenograft models and lung adenocarcinoma cell lines. Transcriptome profiling revealed CCL2 blockade could be responsible for Anlotinib-induced anti-angiogenesis. NCI-H1975 derived xenograft model demonstrated Anlotinib-induced CCL2 blockade play an important role in anti-angiogenesis. Conclusions: This study not only offered the first evidence that Anlotinib inhibits angiogenesis via blocking CCL2 expression, but also provided a novel theoretical basis for the application of Anlotinib in advanced NSCLC patients.

2018-11-30 | E-MTAB-5997 | biostudies-arrayexpress

Gene expression after human SW982 cells treated with anlotinib by a microarray profiling (Affymetrix)

Project description:Anlotinib could significantly suppresses synovial sarcoma proliferation in PDTX model and cell lines. To identify potential anlotinib targets in synovial sarcoma, we performed a microarray profiling (Affymetrix) in human SW982 cells treated with anlotinib.

2019-01-01 | GSE109468 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data