Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis of multiple myeloma cells (HB, KB) and cells (HA, KA) that were not sorted by microfluidic chip

ABSTRACT: Transcriptome sequencing was used to analyze changes in related signaling pathways and gene expression in colon cancer cells when SRD5A1 was knocked down.

ORGANISM(S): Homo sapiens

PROVIDER: GSE189310 | GEO | 2024/11/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptome analysis of multiple myeloma cells (HB, KB) and cells (HA, KA) that were not sorted by microfluidic chip

Project description:Transcriptome analysis of multiple myeloma cells (HB, KB) and cells (HA, KA) that were not sorted by microfluidic chip

| PRJNA782496 | ENA

Down-regulation of SRD5A1 induces autophagy and apoptosis in multiple myeloma

Project description:Steroid 5α-reductase type I (SRD5A1) is a validated oncogene in many sex hormone-related cancers, but its role in multiple myeloma (MM) remains unknown. Based on gene expression profiling of sequential MM samples during disease course, we found that high SRD5A1 expression was correlated with progression and poor prognosis in MM patients. In this study, we assessed the SRD5A1 function in promoting MM cell growth, cell cycle and tumorigenesis by using different human MM cell lines, the xenograft mouse and 5TMM mouse models. Applying lentivirus-mediated short-hairpin RNA (shRNA) method, inducible knockdown of SRD5A1 inhibited myeloma cell growth and induced cell apoptosis as well as autophagy. Meanwhile, the SRD5A1 knockdown-induced apoptosis was aggravated by the autophagy inhibitor 3-methyladenine. Mechanistically, SRD5A1 downregulation simultaneously regulated both the Bcl-2 family proteins mediated apoptosis and the autophagic process via PI3K/Akt/mTOR signaling pathway in MM cells. We also evaluated the therapeutic effect of SRD5A1 inhibitor, Dutasteride, on improving the survival rate of MM mouse model. To summarize, our findings demonstrate that SRD5A1 may serve as a biomarker for MM progression and prognosis, indicating that the dual autophagy-apoptosis regulatory SRD5A1 is a potential target for future therapies in MM patients.

2021-03-03 | GSE155858 | GEO

Transcriptome analysis of SRD5A1 knockdown (Dox) and control (KD) in colorectal cancer

Project description:Transcriptome sequencing was used to analyze changes in related signaling pathways and gene expression in colon cancer cells when SRD5A1 was knocked down.

2020-03-25 | GSE147456 | GEO

Down-regulation of SRD5A1 induces autophagy and apoptosis in multiple myeloma

Project description:Down-regulation of SRD5A1 induces autophagy and apoptosis in multiple myeloma

| PRJNA655885 | ENA

HB-EGF-EGFR Signaling in Bone Marrow Endothelial Cells Mediates Angiogenesis Associated with Multiple Myeloma.

Project description:Epidermal growth factor receptor (EGFR) and its ligand heparin-binding EGF-like growth factor (HB-EGF) sustain endothelial cell proliferation and angiogenesis in solid tumors, but little is known about the role of HB-EGF-EGFR signaling in bone marrow angiogenesis and multiple myeloma (MM) progression. We found that bone marrow endothelial cells from patients with MM express high levels of EGFR and HB-EGF, compared with cells from patients with monoclonal gammopathy of undetermined significance, and that overexpressed HB-EGF stimulates EGFR expression in an autocrine loop. We also found that levels of EGFR and HB-EGF parallel MM plasma cell number, and that HB-EGF is a potent inducer of angiogenesis in vitro and in vivo. Moreover, blockade of HB-EGF-EGFR signaling, by an anti-HB-EGF neutralizing antibody or the EGFR inhibitor erlotinib, limited the angiogenic potential of bone marrow endothelial cells and hampered tumor growth in an MM xenograft mouse model. These results identify HB-EGF-EGFR signaling as a potential target of anti-angiogenic therapy, and encourage the clinical investigation of EGFR inhibitors in combination with conventional cytotoxic drugs as a new therapeutic strategy for MM.

| S-EPMC7017291 | biostudies-literature

Transcriptome analysis of YTHDF2 kockdown(KD) and wildtype(WT) cells in Multiple Myeloma

Project description:RNA-seq experiments was conducted to analyze changes in related signaling pathways and gene expression in colon cancer cells when YTHDF2 was knocked down.

2022-06-30 | GSE162753 | GEO

Classical and/or alternative NF-kB pathway activation in multiple myeloma pathogenesis

Project description:Mutations involving the NFKB pathway are present in at least 17% of multiple myeloma (MM) tumors and 40% of MM cell lines (MMCL). These mutations, which are thought to be progression events, enable MM tumors to become less dependent on extrinsic bone marrow signals that activate NFKB. Studies on a panel of 50 MMCL provide some clarification of the mechanisms through which these mutations act and the significance of classical vs alternative activation of NFKB. First, only one mutation (NFKB2) selectively activates the alternative pathway, whereas several mutations (CYLD, NFKB1, TACI) selectively activate the classical pathway. However, most mutations affecting NIK level (NIK, TRAF2, TRAF3, cIAP1&2, CD40) activate the alternative but often both pathways. Second, we confirm the critical role of TRAF2 in regulating NIK degradation, whereas TRAF3 enhances but is not essential for cIAP1/2-mediated proteosomal degradation of NIK in MM. Third, using transfection to selectively activate the classical or alternative NFKB pathways, we show virtually identical changes in gene expression in one MMCL, whereas the changes are similar albeit non-identical in a second MMCL. Together, our results suggest that MM tumors can achieve increased autonomy from the bone marrow microenvironment by mutations that activate either NFKB pathway.

2009-09-11 | GSE18047 | GEO

Genome-wide maps of chromatin state in YTHDF2 kockdown(KD) and wildtype(WT) cells in Multiple Myeloma

Project description:We found that the experssion of STAT5A was upregulated when the YTHDF2 was knocked down. To identify the function of STAT5A protein as a Transcription factor in YTHDF2 kockdown(KD) and wildtype(WT) cells in Multiple Myeloma. CHIP-seq was conducted to analyze changes in related signaling pathways and gene expression in Multiple Myeloma cells when YTHDF2 was knocked down.

2022-06-30 | GSE163138 | GEO

Subtype-selective positive modulation of K<sub>Ca</sub> 2 channels depends on the HA/HB helices.

Project description:Background and purposeIn the activated state of small-conductance Ca2+ -activated potassium (KCa 2) channels, calmodulin interacts with the HA/HB helices and the S4-S5 linker. CyPPA potentiates KCa 2.2a and KCa 2.3 channel activity but not the KCa 2.1 and KCa 3.1 subtypes.Experimental approachSite-directed mutagenesis, patch-clamp recordings and in silico modelling were utilised to explore the structural determinants for the subtype-selective modulation of KCa 2 channels by CyPPA.Key resultsMutating residues in the HA (V420) and HB (K467) helices of KCa 2.2a channels to their equivalent residues in KCa 3.1 channels diminished the potency of CyPPA. CyPPA elicited prominent responses on mutant KCa 3.1 channels with an arginine residue in the HB helix substituted for its equivalent lysine residue in the KCa 2.2a channels (R355K). KCa 2.1 channels harbouring a three-amino-acid insertion upstream of the cognate R438 residues in the HB helix showed no response to CyPPA, whereas the deletion mutant (KCa 2.1_ΔA434/Q435/K436) became sensitive to CyPPA. In molecular dynamics simulations, CyPPA docked between calmodulin C-lobe and the HA/HB helices widens the cytoplasmic gate of KCa 2.2a channels.Conclusion and implicationsSelectivity of CyPPA among KCa 2 and KCa 3.1 channel subtypes relies on the HA/HB helices.

| S-EPMC8799485 | biostudies-literature

Multiple myeloma

Project description:Multiple myeloma

| PRJNA515992 | ENA