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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.

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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

Circular RNA circTNK2 contributes to immune evasion and acts as a nanotherapeutic target in tamoxifen-resistant ER-positive breast cancer

Project description:circTNK2, a circular RNA, is significantly overexpressed in tamoxifen-resistant breast cancer tissues and is linked to poor prognosis. circTNK2 encodes a novel 487-amino acid protein, termed C-TNK2-487aa, which inhibits the recruitment of natural killer (NK) cells. Mechanistic studies reveal that C-TNK2-487aa interacts with STAT3 and promotes its phosphorylation in ER-positive breast cancer cells. The increased phosphorylated STAT3 then competes with STAT1 binding, inhibiting the formation of STAT1 homodimers required for CXCL10 transcription, ultimately leading to immune evasion. Additionally, circTNK2 binds to SRSF1 and promotes tamoxifen resistance and breast cancer cell proliferation. Co-delivery of circTNK2 antisense oligonucleotides (ASO) and CXCL10 plasmid DNA mediated by BC-targeting ZIF-8 nanoparticles markedly suppresses breast cancer growth, reverses tamoxifen resistance, and increases tumor infiltration of CD56+ NK cells in vivo. These findings underscore the critical role of the circTNK2-encoded peptide in tamoxifen resistance and immune evasion, providing a therapeutic vulnerability in treating tamoxifen-resistant breast cancer.

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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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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.

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

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