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Macropinocytosis requires Gal-3 in a subset of patient-derived glioblastoma stem cells

ABSTRACT: Macropinocytosis requires Gal-3 in a subset of patient-derived glioblastoma stem cells

PROVIDER: PRJNA727010 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14408544.fastq.gz	Fastqsanger.gz
	SRR14408545.fastq.gz	Fastqsanger.gz
	SRR14408546.fastq.gz	Fastqsanger.gz
	SRR14408547.fastq.gz	Fastqsanger.gz
	SRR14408548.fastq.gz	Fastqsanger.gz

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Macropinocytosis requires Gal-3 in a subset of patient-derived glioblastoma stem cells

Project description:GBM cells were treated with GAL3 shRNA vs sh ctrl. Gal3 forms a complex with Rab10 to potentiate macropinocytosis in the mesenchymal subpopulation of GBM tumors

2021-05-04 | GSE173784 | GEO

Macropinocytosis requires Gal-3 in a subset of patient-derived glioblastoma stem cells.

Project description:Recently, we involved the carbohydrate-binding protein Galectin-3 (Gal-3) as a druggable target for KRAS-mutant-addicted lung and pancreatic cancers. Here, using glioblastoma patient-derived stem cells (GSCs), we identify and characterize a subset of Gal-3high glioblastoma (GBM) tumors mainly within the mesenchymal subtype that are addicted to Gal-3-mediated macropinocytosis. Using both genetic and pharmacologic inhibition of Gal-3, we showed a significant decrease of GSC macropinocytosis activity, cell survival and invasion, in vitro and in vivo. Mechanistically, we demonstrate that Gal-3 binds to RAB10, a member of the RAS superfamily of small GTPases, and β1 integrin, which are both required for macropinocytosis activity and cell survival. Finally, by defining a Gal-3/macropinocytosis molecular signature, we could predict sensitivity to this dependency pathway and provide proof-of-principle for innovative therapeutic strategies to exploit this Achilles' heel for a significant and unique subset of GBM patients.

| S-EPMC8192788 | biostudies-literature

A molecularly distinct subset of glioblastoma requires serum-containing media to establish sustainable bona fide glioblastoma stem cell cultures

Project description:A molecularly distinct subset of glioblastoma requires serum-containing media to establish sustainable bona fide glioblastoma stem cell cultures

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RNA-seq of genetically engineered mouse EGFR positive glioblastoma tumors with PDGFRA and GAL-1 positive and negative populations

Project description:RNA-seq of genetically engineered mouse EGFR positive glioblastoma tumors flow cytometry sorted into PDGFRA and GAL-1 positive and negative populations.

2022-04-06 | GSE195813 | GEO

Cell polarity proteins promote macropinocytosis in response to metabolic stress

Project description:Macropinocytosis has emerged as a nutrient-scavenging pathway that cancer cells exploit to survive the nutrient-deprived conditions of the tumor microenvironment. Cancer cells are especially reliant on glutamine for their survival, and in pancreatic ductal adenocarcinoma (PDAC) cells, glutamine deficiency can enhance the stimulation of macropinocytosis, allowing the cells to escape metabolic stress through the production of extracellular-protein-derived amino acids. Here, we identify the atypical protein kinase C (aPKC) enzymes, PKC and PKCas novel regulators of macropinocytosis. In normal epithelial cells, aPKCs are known to regulate cell polarity in association with the scaffold proteins Par3 and Par6, controlling the function of several targets, including the Par1 kinases. In PDAC cells, we identify that each of these cell polarity proteins are required for glutamine stress-induced macropinocytosis. Mechanistically, we find that the aPKCs are regulated by EGFR signaling or by the transcription factor CREM to promote the relocation of Par3 to microtubules, facilitating macropinocytosis in a dynein-dependent manner. Importantly, we determine that cell fitness impairment caused by aPKC depletion is rescued by the restoration of macropinocytosis and that aPKCs support PDAC growth in vivo. These results identify a previously unappreciated role for cell polarity proteins in the regulation of macropinocytosis and provide a better understanding of the mechanistic underpinnings that control macropinocytic uptake in the context of metabolic stress.

2024-10-22 | GSE276007 | GEO

RNA-seq of wild-type, Gal-1 knockout, Gal-3 knockout and Gal-1/Gal-3 double knockout mouse embryonic stem cells (mESC) deprived of LIF for 7 days

Project description:Galectin-1 (Gal-1) and Galectin-3 (Gal-3) are conserved carbohydrate-binding proteins that also display RNA-binding activity. We generated mouse embryonic stem cells (mESC) constitutively depleted of Gal-1 and/or Gal-3 using CRISPR-Cas9, and assessed the transcriptomic effects of the individual or concomitant depletion of Gal-1 and Gal-3 in mESCs differentiated by deprivation of the leukaemia inhibitory factor (LIF) for 7 days. Wild-type cells were employed as control.

2023-05-27 | E-MTAB-9262 | biostudies-arrayexpress

Vibrio harveyi strain:Gal 88 | isolate:Gal 88

Project description:Vibrio harveyi strain:Gal 88 | isolate:Gal 88 Genome sequencing

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Progestin receptor promotes cell macropinocytosis through CDC42 in pancreatic cancer

Project description:Endocrine receptors play an essential role in tumor metabolic reprogramming and represent a potential therapeutic approach in pancreatic ductal adenocarcinoma (PDAC). PDAC is characterized by a nutrient-deprived microenvironment, and to support their energetic needs, they can internalize extracellular proteins via macropinocytosis. In this study, we found that progesterone receptor (PGR), a steroid-responsive nuclear receptor, has a higher expression in PDAC tissues from patients and transgenic LSL-KrasG12D/+; LSL-Trp53R172H/+; PDX1-cre (KPC) mice. Moreover, PGR knockdown restrained PDAC cell survival and tumor growth both in vitro and in vivo. Genetic and pharmacological PGR inhibition resulted in dramatically macropinocytosis impairment in PDAC cells and subcutaneous tumor models, which indicates involvement of this receptor in macropinocytosis regulation. Mechanistically, PGR deficiency caused a subsequently decreased expression of CDC42, a key regulator in macropinocytosis. These data deepen our understanding of how endocrine system influences tumor progression via non-classical pathway and provide a novel therapeutic option for patients with PDAC.

2023-09-27 | GSE228301 | GEO

GPNMB+Gal-3+ Hepatic Parenchymal Cells Promote Immunosuppressive Microenvironment Formation and Hepatocellular Carcinogenesis

Project description:Hepatocellular carcinoma (HCC) involves a multistep pathological process in which heterogenous cells are evolved to shape an immunosuppressive microenvironment. Yet it remains largely unknown regarding the specific cell populations and their evolving routes essential for HCC development. Here, we created a rat model mimicking human HCC and generated a single-cell resolution atlas to HCC development. Specifically, we identified three populations of hepatic parenchymal cells during HCC progression, i.e., metabolic hepatocyte (HC Meta ), hepatic progenitor cell-like population with differentiation potential (HPC-like Diff ) and immunosuppressive malignant transformation subset (H-M Immu ). These three distinct subpopulations formed an oncogenic trajectory depicting a dynamic landscape of hepatocyte carcinogenesis, with signature genes reflecting the transition from HPC-like Diff to H-M Immu . Cross-species comparative analysis further revealed the H-M Immu subset to be highly conserved. Importantly, the H-M Immu (GPNMB + Gal-3 + ) cells exhibit both malignant and immunosuppressive properties. Moreover, SOX18 was found to be required for the generation of GPNMB + Gal-3 + H-M Immu cells and for their ability to form tumors. Enrichment of GPNMB + Gal-3 + H-M Immu subset was found to be associated with poor prognosis and higher rate of recurrence for HCC patients. Collectively, we unraveled the single-cell evolving mechanism of HCC and uncovered GPNMB + Gal-3 + H-M Immu cells as a major subset contributing to the immunosuppressive microenvironment and HCC malignance

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GPNMB+Gal-3+ Hepatic Parenchymal Cells Promote Immunosuppressive Microenvironment Formation and Hepatocellular Carcinogenesis.

2024-01-02 | GSE243688 | GEO