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Tumor cell-derived CTSZ mediates macrophage recruitment and M2 polarization to promote castration-resistant prostate cancer progression through the TRA2A/IL-32/ITGA5 axis

ABSTRACT: Tumor cell-derived CTSZ mediates macrophage recruitment and M2 polarization to promote castration-resistant prostate cancer progression through the TRA2A/IL-32/ITGA5 axis

PROVIDER: PRJNA1035467 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26664975_1.fastq.gz	Fastqsanger.gz
	SRR26664975_2.fastq.gz	Fastqsanger.gz
	SRR26664976_1.fastq.gz	Fastqsanger.gz
	SRR26664976_2.fastq.gz	Fastqsanger.gz
	SRR26664977_1.fastq.gz	Fastqsanger.gz

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Tumor cell-derived CTSZ mediates macrophage recruitment and M2 polarization to promote castration-resistant prostate cancer progression through the TRA2A/IL-32/ITGA5 axis

Project description:Castration-resistant prostate cancer (CRPC) is a lethal stage of prostate cancer after androgen deprivation therapy (ADT). However, most studies have focused on the autonomous alterations of CRPC cells, and the specific contribution of CRPC cells to the metastatic microenvironment remains less well understood. Here, we report that cathepsin Z (CTSZ) was overexpressed in CRPC cells, enhancing macrophage infiltration and promoting M2 polarization, ultimately leading to the metastasis of CRPC. Mechanistically, CTSZ facilitates the maturation of IL-32 mRNA by directly degrading the alternative splicing factor TRA2A in CRPC cells, thereby increasing the secretion of IL-32. Subsequently, elevated IL-32 directly binds to ITGA5 in macrophages and activates the PI3K/AKT/mTOR pathway in macrophages, thus promoting the recruitment and polarization of macrophages. Furthermore, treatment with an ITGA5 inhibitor blocked the effect of CTSZ overexpression and suppressed CRPC development. These findings uncover a novel mechanism wherein CTSZ involvement in cell‒cell interactions within the tumor microenvironment contributes to the progression of CRPC and provide new therapeutic strategies for CRPC.

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The scaffolding role of RNA in ribonucleoprotein complexes: TRA2A recruitment in FXTAS disease

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Project description:Paralogs often exhibit functional redundancy, allowing them to effectively compensate for each other's loss. However, this buffering mechanism is frequently disrupted in cancer, exposing unique paralog-specific vulnerabilities. Here, we identify a selective dependency on the splicing factor TRA2A. We find that TRA2A and its paralog TRA2B are synthetic lethal partners that function as widespread and largely redundant activators of both alternative and constitutive splicing. While loss of TRA2A alone is typically neutral due to compensation by TRA2B, we discover that a subset of cancer cell lines are highly TRA2A-dependent. Upon TRA2A depletion, these cell lines exhibit a lack of paralog buffering specifically on shared splicing targets, leading to defects in mitosis and cell death. Notably, TRA2B overexpression rescues both the aberrant splicing and lethality associated with TRA2A loss, indicating that paralog compensation is dosage-sensitive. Together, these findings reveal a complex dosage-dependent relationship between paralogous splicing factors, and highlight how dysfunctional paralog buffering can create a selective dependency in cancer.

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Project description:The RNA-binding protein Transformer 2 alpha homolog (TRA2A), previously identified as an alternative splicing factor, was reported as a crucial oncogene in recent years. However, the underlying mechanisms are poorly understood. In this study, we found that TRA2A is highly up-regulated in glioblastoma and is significantly correlated with clinical diagnosis and prognosis. We verified that TRA2A promotes the proliferation and metastasis of glioblastoma. Epitranscriptomic profiling further revealed Interferon-induced protein with tetratricopeptide repeat 1/2/3 (IFIT1/2//3) as the key RNA targets mediated by TRA2A, which further over-activates the EGFR-AKT signaling pathway by enhancing the recycling of p-EGFR. This work reveals a novel oncogenic mechanism of TRA2A in glioblastoma.

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The scaffolding role of RNA in ribonucleoprotein complexes: TRA2A recruitment in FXTAS disease

Project description:The scaffolding role of RNA in ribonucleoprotein complexes: TRA2A recruitment in FXTAS disease

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Paraburkholderia sp. 32 strain:32

Project description:Paraburkholderia sp. 32 strain:32 Genome sequencing

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Xylella fastidiosa 32 strain:32

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Interleukin-32 is progressively expressed in Mycosis Fungoides independent of helper T-cell 2 and helper T-cell 9 polarization

Project description:Mycosis Fungoides (MF) is typically characterized by a mature CD4+ memory T-cell phenotype, and regarded as a helper T-cell (Th)2-skewed disease. Here, using skin samples from MF (n=21), healthy volunteers (n=17), atopic dermatitis (n=17), and psoriasis (n=9), we performed RT-PCR to show highest interleukin (IL)-32 mRNA expression in MF compared to benign inflammatory diseases, and its increasing expression with disease progression. By immunohistochemistry and immunofluorescence, we confirmed IL-32 protein expression by numerous CD3+CD4+ T-cells and some epidermotropic T-cells in MF lesions. IL-32 is expressed by MyLa cells (MF cell line) and promoted their proliferation and viability in a dose-dependent fashion. IL-32-treated MyLa and HH cells (CTCL cell line) showed upregulation of cell proliferation and survival genes. Of major 'polar' T-cell cytokines, only IFN-γ mRNA increases with MF progression and positively correlates with IL-32 mRNA expression levels. Th2 cytokines do not show consistent increases with MF progression nor positive correlation with IL-32 mRNA expression levels. Furthermore, by flow cytometry, IL-32 production by circulating activated T-cells in healthy individulas was found in IFN-γ+ and IFN-γ- cells but not in IL-4+ or IL-13+ cells. In conclusion, we identified IL-32+ cells as likely tumor cells in MF, and clearly showed that IL-32 mRNA expression levels increase with MF progression. We found that IL-32 mRNA expression levels in MF are significantly higher than those in other skin diseases, and that some IL-32+ T-cells are independent from defined Th subsets. Thus IL-32 may play a unique role in MF progression as an autocrine cytokine.

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