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

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

PROVIDER: PRJNA992569 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25195454.fastq.gz	Fastqsanger.gz
	SRR25195455.fastq.gz	Fastqsanger.gz
	SRR25195456.fastq.gz	Fastqsanger.gz
	SRR25195457.fastq.gz	Fastqsanger.gz
	SRR25195458.fastq.gz	Fastqsanger.gz

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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

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

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.

2020-10-01 | GSE150291 | GEO

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

2015-12-16 | GSE76020 | GEO

Mechanism of Kindlin-2 regulating invasion and metastasis of human Hepatocellular carcinoma

Project description:To explore the mechanism of Kindlin-2 regulating invasion and metastasis of human Hepatocellular carcinoma, we performed gene expression microarray analysis on Kindlin-2 knockdown LM3 cells and the control cells to compare the gene expression levels between the two groups.

2017-04-19 | GSE97951 | GEO

Kindlin-2/Moesin interaction orchestrates sprouting angiogenesis via modulating endothelial membrane mechanics and VEGF signaling

Project description:Membrane mechanics play a crucial role in cellular signaling and fate determination, yet their impact on angiogenesis remains poorly understood. Here, we identify Kindlin-2 as a key regulator of sprouting angiogenesis via regulating endothelial membrane tension through its interaction with Moesin, a crucial linker protein between the cell membrane and the actin cortex, a process crucial for sprouting angiogenesis. Mechanistically, Kindlin-2 binds to the N62 residue of Moesin, limiting its overactivation and maintaining proper membrane tension to facilitate VEGFR2 endocytosis and downstream signaling. Using both developmental and pathological models, we demonstrate that the interaction of Kindlin-2 and Moesin is enhanced in high angiogenic conditions, and endothelial Kindlin-2 deletion reduces angiogenesis. Furthermore, mutation of Moesin at N62 phenocopies the effects of Kindlin-2 loss. Together, these findings uncover a previously unrecognized mechanism linking membrane tension regulation to angiogenesis and provide new insights into targeting the Kindlin-2–Moesin axis for therapeutic intervention in neovascular diseases.

2025-07-23 | GSE302986 | GEO

Involvement of Kindlin-1 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 (cSCC). Here we show in non-KS-associated patients that elevation of FERMT1 expression is increased in actinic keratoses compared to normal skin, with a further increase in cSCC supporting a pro-tumorigenic role in this population. In contrast, we show that loss of Kindlin-1 leads to increased SCC tumor growth in vivo and in 3D spheroids, which was associated with the development of a hypoxic tumor environment and increased glycolysis. The metalloproteinase Mmp13 was upregulated in Kindlin-1-depleted tumors, and increased expression of MMP13 was responsible for driving increased invasion of the Kindlin-1-depleted SCC cells. These results provide evidence that Kindlin-1 loss in SCC can promote 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.

| S-EPMC11233684 | biostudies-literature

Kindlin-2 Orchestrates brown adipose tissue maintenance and thermogenic programing

Project description:Analyze the internal gene changes in brown adipocytes after knockout of Kindlin-2

2025-08-31 | GSE306089 | GEO

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

Comparative gene expression profiling of group-housed, less aggressive vs. single-housed, more aggressive male flies

Project description:Social experience influences multiple behaviors of many animal species, including aggression. Social isolation often increases aggressiveness. To investigater the molecular basis of social influences on aggressiveness, we performed comparative gene expression profiling on heads from 6-day-old, single-housed, more aggressive and group-housed, less aggressive male flies. Keywords: social experience

2008-02-08 | GSE6994 | GEO

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