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Role of Kindlin-2 in breast cancer immune evasion

ABSTRACT: Role of Kindlin-2 in breast cancer immune evasion

PROVIDER: PRJNA1219181 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32229515_1.fastq.gz	Fastqsanger.gz
	SRR32229515_2.fastq.gz	Fastqsanger.gz
	SRR32229516_1.fastq.gz	Fastqsanger.gz
	SRR32229516_2.fastq.gz	Fastqsanger.gz

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Role of Kindlin-2 in breast cancer immune evasion

Project description:Kindlin-2 (K2) plays a major role in driving TNBC tumors progression and metastasis through the regulation of several hallmarks of cancer. We have employed a single cell RNA sequencing approach using 10x Genomics scRNAseq to study the role of Kindlin-2 in immune evasion of TNBC tumors. Tumors derived from control 4T1 cells or their K2-KO derivatives grown in syngeneic immune competent BALB/c mine werw subjected to scRNAseq to indentify the efect of loss of K2 on the tumor immune environment.

2025-02-04 | GSE288744 | GEO

Expression data of cDNA from the ACHN control and Kindlin-2-depleting cells

Project description:Kindlin-2, an integrin-interacting FERM-domain-containing protein, has been known to play critical roles for tumor progression. However, the role of Kindlin-2 in renal cell carcinoma (RCC) progression has not been reported. We aim to investigate the role of Kindlin-2 in the progression of RCC and the underlying mechanisms. To uncover the related pathway in which Kindlin-2 is involved to promote clear cell renal cell carcinoma progression, ACHN control and Kindlin-2-depleting cells were analyzed by Affymetrix GeneChip human Gene 1.0 ST Arrays. ACHN cells were transfected with control short hairpin RNA (shRNA) or Kindlin-2 shRNA. ACHN control and Kindlin-2-depleting cells cDNAs were hybridized to Affymetrix GeneChip Human Gene 1.0 ST arrays. Data were analyzed by Expression Console 1.4.1.

2015-12-16 | E-GEOD-76020 | biostudies-arrayexpress

PI3Kβ controls immune evasion in PTEN-deficient breast tumors

Project description:PI3Kβ controls immune evasion in PTEN-deficient breast tumors

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PI3Kβ controls immune evasion in PTEN-deficient breast tumors

Project description:PI3Kβ controls immune evasion in PTEN-deficient breast tumors

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Expression data of cDNA from the ACHN control and Kindlin-2-depleting cells

2015-12-16 | GSE76020 | GEO

Breast Cancer Stem Cells Regulated Metabolism Remodeling of Bulk Tumor Cells Drives Immune Evasion

Project description:Reprogramming of energy metabolism plays pivotal roles in cancer progression and immune surveillance. Here, we demonstrated that breast cancer cells showed positive feedback enhanced aerobic glycolysis in hypoxia condition. Further investigation suggested that breast cancer stem cells (BCSCs) induced by hypoxia stimulate aerobic glycolysis in bulk tumor cells. Cells cultured with hypoxic tumor cell- or BCSC-secretome exhibited similar gene expression patterns, with global remodeling of metabolism pathways, particularly glycolysis. BCSCs regulated glycolysis promoted breast cancer progression and evasion of immune surveillance. Screening of BCSC secretome identified MIF as a pivotal factor that potentiated glycolysis by increasing the expression of ALDOC. Breast cancer cell–intrinsic MIF depletion inhibited tumor progression and augmented intratumoral cytolytic CD8+ T cells and pro-inflammatory macrophages. Targeting MIF optimized immune checkpoint therapy of breast cancer in both syngeneic mouse models and humanized mouse model. Hence, this study delineates the contribution of BCSC regulated bulk tumor cell glycolysis in immune surveillance; and thereby proposes strategies to optimize immunotherapy in breast cancer.

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Kindlin-2 modulates PTH1R to regulate bone mass and PTH actions in bone

Project description:To investigation the role of PTH and Kindlin-2 in bone development, we performed single-cell RNA-sequencing. From Con-veh, Con-PTH, cKO-veh, cKO-PTH, we profiled more than 20k single cells, including multi-potent mesenchymal stromal cells (MSC), osteoprogenitors, osteoblasts, chondrocytes, fibroblasts, endothelial cells, smooth muscle cells, skeletal muscle cells, pericytes, and schwann cells. We found proportion of part of these cells were significant altered by PTH or Kindlin-2 loss, especially for MSC, osteoblast, chondrocyte, and fibroblast. Transcriptomic analysis revealed gene expression was dramatically regulated by PTH or Kindlin-2 loss.

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Lactate sensing drives fungal immune evasion

Project description:Lactate sensing drives fungal immune evasion

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The tumor intrinsic role of the m6A reader YTHDF2 in regulating immune evasion

Project description:The tumor intrinsic role of the m6A reader YTHDF2 in regulating immune evasion

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Loss of Kindlin-1 drives a more aggressive phenotype in cutaneous squamous cell carcinoma

Project description:Kindler syndrome (KS) is a rare genodermatosis resulting from loss-of-function mutations in FERMT1, the gene that encodes Kindlin-1. KS patients have a high propensity to develop aggressive and metastatic cutaneous squamous cell carcinoma (SCC). In this study, we show that loss of Kindlin-1 in a mouse model of cutaneous SCC leads to increased migration, invasion and degradation of collagen. Loss of Kindlin-1 increased tumor growth in vivo and in 3D spheroids, which was associated with the development of a hypoxic tumor environment and increased glycolysis. One of the most highly upregulated genes in Kindlin-1-depleted tumors was Mmp13, and the increased expression of MMP13 was responsible for driving the increased migration and invasion of the Kindlin-1-depleted SCC cells. These results provide evidence that Kindlin-1 loss in SCC can promote migration and invasion through the upregulation of MMP13, and offer novel insights into how Kindlin-1 loss leads to the development of a hypoxic environment that is permissive for tumor growth.

2023-07-14 | GSE236883 | GEO

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