Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic profiling of GOLM1 silenced A549 lung adenocarcinoma cells

ABSTRACT: GOLM1 is a Golgi-resident protein implicated in multiple cancers, but its role in lung adenocarcinoma remains incompletely understood. RNA sequencing was performed on A549 lung adenocarcinoma cells following siRNA-mediated silencing of GOLM1 using two independent siRNAs and a non-targeting control. Differential gene expression analysis was conducted to identify molecular pathways regulated by GOLM1 depletion, including alterations in cell cycle regulation, DNA replication, lysosomal pathways, and mitochondrial-associated processes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE337173 | GEO | 2026/07/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

GOLM1 dictates acquired Lenvatinib resistance by a GOLM1-CSN5 positive feedback loop upon EGFR signaling activation in hepatocellular carcinoma

Project description:Lenvatinib is a multiple receptor tyrosine kinases inhibitor (TKI) authorized for first-line treatment of hepatocellular carcinoma (HCC). However, Lenvatinib resistance is common in HCC clinical treatment, highlighting the urgent need to understand mechanisms of resistance. Here, we identified Golgi membrane protein 1 (GOLM1), a type II transmembrane protein originally located in the Golgi apparatus, as a novel regulator of Lenvatinib resistance. We established Lenvatinib resistance in human HCC cell lines PLC/PRF/5. Through RNA-seq, we found that GOLM1 was significantly upregulated, which was further validated in patients derived tumor tissue and peripheral blood. GOLM1 overexpression contributes to Lenvatinib resistance and HCC progression in vitro and in vivo. Mechanistically, GOLM1 upregulates CSN5 expression through EGFR-STAT3 pathway. Reversely, CSN5 deubiquitinates and stabilizes GOLM1 protein by inhibiting ubiquitin-proteasome pathway of GOLM1. Collectively, our data demonstrate that GOLM1 is one of the key driver of Lenvatinib resistance in HCC and depicts a molecular network in Lenvatininb resistant HCC cells.

2024-08-07 | GSE273819 | GEO

Targeted Ubiquitination and Degradation of GOLM1 by CC-885 Suppresses Hepatocellular Carcinoma Growth and Metastasis

Project description:Hepatocellular carcinoma (HCC) is a leading cause of cancer mortality, necessitating innovative therapeutic approaches. This study demonstrates that the compound CC-885 exerts potent anti-tumor effects in HCC both in vitro and in vivo. CC-885 significantly inhibited proliferation, migration, and invasion of HCC cells. In vivo, CC-885 markedly reduced tumor growth and angiogenesis in chick embryo and mouse xenograft models. Mechanistically, CC-885 selectively reduced GOLM1 protein levels via ubiquitin-mediated proteasomal degradation, without affecting its mRNA levels. GOLM1 knockdown mimicked the anti-proliferative effects of CC-885, while overexpression of GOLM1 conferred resistance to CC-885-induced apoptosis and growth inhibition. CC-885 facilitated the interaction between GOLM1 and the E3 ubiquitin ligase CRBN, promoting GOLM1 ubiquitination and degradation. Transcriptomic analyses revealed that CC-885 and GOLM1 knockdown modulated key pathways involved in apoptosis, NF-κB signaling, and cell proliferation. These findings highlight CC-885 as a promising therapeutic agent for HCC, primarily by facilitating the CRBN-dependent degradation of GOLM1, underscoring its potential for clinical application.

2024-10-11 | GSE272556 | GEO

Aberrant expression of GOLM1 protects ALK+ anaplastic large cell lymphoma from apoptosis by enhancing BCL-XL stability

Project description:GOLM1 suppresses ALCL apoptosis in ALCL

2023-02-20 | GSE224914 | GEO

MicroRNA expression data from Bcl-xL silenced A549 lung adenocarcinoma cells

2013-05-18 | GSE47059 | GEO

Proteomic Analysis of Huh7, HIEC6, and NCI-H295R cells using High-affinity anti-Golm1 mAb by IP-MS.

Project description:we conducted IP-MS strategy to screen its interacting proteins. High-affinity anti-Golm1 mAb and IgG were used in multiple cell lines including Huh7, HIEC6, and NCI-H295R cells. Proteins with more than two peptide segments enriched or exclusively within the Golm1 group were identified as putative interacting partners of Golm1.

2026-03-23 | PXD061115 | Pride

MicroRNA expression data from Bcl-xL silenced A549 lung adenocarcinoma cells

Project description:Bcl-xL is an anti-apoptotic protein that is frequently found to be overexpressed in non-small cell lung cancer leading to an inhibition of apoptosis and poor prognosis. Recently, the role of miRNAs in regulating apoptosis and cell survival during tumorigenesis has become evident, with cancer cells showing perturbed expression of various miRNAs. We utilized miRNA microarrays to determine if miRNA dysregulation in bcl-xL silenced lung adenocarcinoma cells could be involved in regulating apoptotic behavior, and identified dysregulated miRNAs with putative targets involved in signal transduction pathways regulating apoptosis, cell proliferation and cell progression. Short interfering RNA-based transfection of A549 was carried out inducing a reduction in bcl-xL expression levels. 24 hours post-transfection total RNA was isolated using TRIzol reagent and hybridized onto Affymetrix GeneChip miRNA Arrays. A global miRNA expression profile was then established, which compared total RNA, extracted from siRNA-transfected and non-transfected A549 cells. All experiments were carried out with three independent biological replicates.

2013-05-18 | E-GEOD-47059 | biostudies-arrayexpress

Project description:Transcriptomic profiling of GOLM1 silenced A549 lung adenocarcinoma cells.

| PRJNA1483734 | ENA

GOLM1 dictates acquired Lenvatinib resistance by a GOLM1-CSN5 positive feedback loop upon EGFR signaling activation in hepatocellular carcinoma

Project description:GOLM1 dictates acquired Lenvatinib resistance by a GOLM1-CSN5 positive feedback loop upon EGFR signaling activation in hepatocellular carcinoma

| PRJNA1143404 | ENA

Differentially expressed genes after miRNA or siRNA transfection in human cancer cell lines (A-498, 786-O, A549, TE-8, PANC-1, SW1990, PC3 and PC3M)

Project description:To identify differentially expressed genes by anti cancer treatments (microRNAs or siRNAs) in human cancer, several cell lines ( renal cell carcinoma, lung adenocarcinoma, esophageal, pancreatic and prostate cancer) were subjected to Agilent whole genome microarrays.

2017-01-08 | GSE93290 | GEO

Differentially expressed genes after miRNA or siRNA transfection in human cancer cell lines (II)

Project description:To identify differentially expressed genes by anti cancer treatments (microRNAs or siRNAs) in human cancer, several cell lines (bladder cancer, prostate cancer, renal cell carcinoma, oral squamous cell carcinoma and lung squamous cell carcinoma) were subjected to Agilent whole genome microarrays. Human cancer cell lines (SAS, HSC3, BOY, T24, PC3, PC3M, DU145, C4-2, 786-O, A-498 and EBC-1) were treated with miRNAs (miR-205, miR-29a, miR-144-3p, miR-144-5p, miR-451, miR-210, miR-145-5p, miR-145-3p, miR-23b cluster, miR-221, miR-222 and miR-223), siRNAs (si-GOLM1, si-HMGB3, si-CENPF, si-LOXL2, si-TMEM184B and si-CORO1C).

2016-04-13 | E-GEOD-66498 | biostudies-arrayexpress

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