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TLR3 overexpression induces invasion of prostate cancer cells, whereas its activation triggers apoptosis

ABSTRACT: TLR3 overexpression induces invasion of prostate cancer cells, whereas its activation triggers apoptosis

PROVIDER: PRJNA771529 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16352000.fastq.gz	Fastqsanger.gz
	SRR16352001.fastq.gz	Fastqsanger.gz
	SRR16352002.fastq.gz	Fastqsanger.gz
	SRR16352003.fastq.gz	Fastqsanger.gz
	SRR16352004.fastq.gz	Fastqsanger.gz

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TLR3 overexpression induces invasion of prostate cancer cells, whereas its activation triggers apoptosis

Project description:Toll-like receptors are proteins that play an important role in the innate immune system. They are frequently detected in immune cells such as macrophages or dendritic cells. Their role has been in part studied in prostate cancer. However, in the present study we focus mostly on their functional significance at various types of cancer therapy resistance.

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Peptide occurring in Enterobacteriaceae triggers Streptococcus pneumoniae apoptosis

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Complete TLR3 deficiency

Project description:The objective of this study is to study the Toll-like receptor 3 (TLR3)-dependent gene expression in human fibroblast cells and peripheral blood mononuclear cells (PBMCs) Fibroblast cells and PBMCs from donors with autosomal recessive (AR) complete TLR3 deficiency and autosomal dominant (AD) partial TLR3 deficiency were collected for microarray analysis to measure the transcriptional responsiveness of TLR3 in fibroblast and PBMCs. A total of 3 healthy controls, 1 AD TLR3-deficient patient, 1 AR TLR3-deficient patient, 1 AR UNC-93B-deficient patient, 1 MyD88 deficient patien were used in this study. The fibroblast cells were cultured in DMEM medium supplemented with 10% fetal calf serum (FCS). The PBMCs were cultured in RPMI medium complemented with 10% FCS. Different kinetics (2 hours and 8 hours) of poly(I:C) (25ug/ml, purchased from Amersham) stimulations were performed, aiming to define TLR3-inducible genes in these human cells. A stimulation of IL-1β (20ng/ml, purchased from R&D system Inc.) was used as a positive activation control with same kinetics of stimulations. A total of one million cells per stimulation were used for fibroblasts, and around 1.5 million cells per stimulation for PBMCs.

2011-11-02 | E-GEOD-30951 | biostudies-arrayexpress

Assessment of the impact of the TLR3 L412F variant in terms of TLR3-sensitive transcript induction

Project description:we assessed the impact of TLR3 L412F at endogenous cellular levels upon double stranded RNA (dsRNA) stimulation, by performing RNA-sequencing in primary fibroblasts from individuals homozygous for the ancestral allele (n =2) or homozygous for TLR3 L412F (n = 4) upon extracellular Poly(I:C) stimulation that activates the TLR3 pathway. The average response of TLR3 L412F homozygotes was significantly decreased (mean Δ log2 fold-change = 0.93; Wilcoxon p <10-16) compared to that of cells with the ancestral allele, approaching that of TLR3-deficient cells, used as negative control.

2023-01-13 | GSE216304 | GEO

Phosphorylated TLR3 nuclear translocation in cancer cell promotes metastasis and chemoresistance

Project description:Aberrant expression and subcellular location of innate sensors in cancer cells, such as Toll-like receptors (TLRs), correlates with pro-tumoral inflammation and cancer progression, but the mechanism is still largely unknown. Deciphering the proinflammatory mediators in tumor microenvironment will contribute to the development of cancer therapeutics. By using immunohistochemistry in pancreatic ductal adenocarcinoma (PDAC) and multiple other cancer samples, here we found that cancer cell TLR3, a well-known cytoplasmic dsRNA sensor, translocated to the nucleus especially upon chemotherapy stress. Nuclear TLR3 increased the invasive and proliferative properties, and inhibited chemotherapy-induced apoptosis of cancer cells in vitro. Meanwhile, mice bearing cancer cells with nuclear TLR3 exhibited increased liver metastasis and shortened survival. Mechanistically, phosphokinase JAK1 was responsible for TLR3 phosphorylation at S155 to induce its nuclear translocation in cooperation with a nuclear transport factor importin α5. Chemotherapeutic stress induced the aberrant aggregation of dsRNA in the nucleus, which potentially contributed to nuclear TLR3 activation. Then nuclear TLR3 recruited protein arginine methyltransferase 5 (PRMT5) and bound to c-Myc to promote symmetrical dimethylation and multimerization of c-Myc, resulting in the activation of c-Myc downstream target genes and pro-tumoral signaling pathways. Accordingly, high levels of cancer cell nuclear TLR3 in clinical samples predicted patients’ worse prognosis with shorter disease-free survival, overall survival and poor response to neoadjuvant chemotherapy. Therefore, the identification of nuclear TLR3 provides new insight into non-classical functions of innate immune sensors in cancer, and JAK1/TLR3/PRMT5/c-Myc axis may sever as a new prognostic indicator and potential therapeutic target to overcome chemoresistance.

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Complete TLR3 deficiency

Project description:The objective of this study is to study the Toll-like receptor 3 (TLR3)-dependent gene expression in human fibroblast cells and peripheral blood mononuclear cells (PBMCs)

2011-11-02 | GSE30951 | GEO

Mitol dysfunction triggers apoptosis of hematopoietic stem cell via ER stress response

Project description:Mitol dysfunction triggers apoptosis of hematopoietic stem cell via ER stress response

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Isorhamnetin Inhibits Proliferation and Invasion and Induces Apoptosis Through the Mitochondria‑Dependent Apoptosis in Human Gastric Cancer Cells

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microRNA expression profiling of small intestine of Tlr3+/+ and Tlr3-/- mice after total body g-irradiation

Project description:Microarray was performed to comprehensively examine microRNA induction in murine small intestine after exposure to total body g-irradiation. Small intestines were collected from Tlr3+/+ and Tlr3-/- mice at 0 and 6 hr after exposure to 10 Gy of total body g-irradiation. Samples were pooled from 3 mice. Total RNA was extracted and subjected to microRNA microarray analysis.

2015-02-01 | E-GEOD-42916 | biostudies-arrayexpress

Siglec-7 inhibits TLR3-induced pro-inflammatory cytokine production from human monocytes and macrophages

Project description:Immune checkpoint receptors, including Sialic-acid-binding immunoglobulinlike lectins (Siglecs), are critical regulators of immune homeostasis. Siglecs can serve as negative regulators of Toll-like receptor (TLR) signaling, promoting the resolution of inflammatory signaling through feedback inhibition mechanisms. Previous studies demonstrated that Siglec-E, the murine homolog of the human inhibitory receptor Siglec-7, negatively regulates TLR4 signaling by controlling receptor endocytosis. This regulatory mechanism suggests that Siglec-7 may also limit TLR signaling. Here we reveal a novel mechanism whereby Siglec-7 represses endosomal TLR3 activation, compared to other TLRs, in human myeloid cells. Crosslinking Siglec-7 with antibody clone QA79 significantly reduced TNFa secretion in U937 cells, primary monocytes, and macrophages following Poly(I:C) stimulation. Mechanistically, QA79 triggers rapid FcgRindependent internalization and endolysosomal trafficking of surface Siglec-7, which enables the direct co-localization of Siglec-7 with TLR3 within the endolysosome. This co-localization between Siglec-7 and TLR3 suppresses NFkB phosphorylation, a key pro-inflammatory signaling node downstream of TLR3. These findings establish a previously unrecognized negative regulatory role of Siglec-7 for TLR3-mediated inflammation in myeloid cells, where a disrupted interaction could contribute to autoimmune disease pathogenesis. Targeting this pathway represents a promising therapeutic approach for TLR3-driven autoimmune diseases.

2026-03-05 | PXD075217 | JPOST Repository

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