Vimentin epigenetic deregulation in Bladder Cancer associates with acquisition of invasive and metastatic phenotype through epithelial-to-mesenchymal transition

Monteiro‐Reis, Sara; Miranda‐Gonçalves, Vera; Guimarães‐Teixeira, Catarina; Martins‐Lima, Cláudia; Lobo, João; Montezuma, Diana; Dias, Paula C.; Neyret‐Kahn, Hélène; Bernard‐Pierrot, Isabelle; Henrique, Rui; Jerónimo, Carmen

doi:10.7150/ijbs.77181

Cited by 6 publications

(1 citation statement)

References 47 publications

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“…For example, H1FX has mainly been highlighted to be associated with cancer to date ( 35 , 36 ), whereas ZFP36L2 was reported to induce apoptosis and inhibit cell proliferation ( 37 , 38 ). VIM is involved in cell attachment, migration, and signal transduction ( 39 ). Here, we separated the exhausted subsets of CD4 + and CD8 + T cells into distinct subclusters via further unsupervised analysis.…”

Section: Discussionmentioning

confidence: 99%

Landscape of Exhausted T Cells in Tuberculosis Revealed by Single-Cell Sequencing

Pan

Zhang

et al. 2023

Microbiol Spectr

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Identifying the changes in immune cells in response to infection can provide a better understanding of the effects of Mycobacterium tuberculosis on the host immune system. We performed single-cell RNA-sequencing analysis of CD4 + T and CD8 + T cells isolated from peripheral blood mononuclear cells of healthy individuals and patients with tuberculosis to reveal the cellular characteristics.

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Section: Discussionmentioning

confidence: 99%

Landscape of Exhausted T Cells in Tuberculosis Revealed by Single-Cell Sequencing

Pan

Zhang

et al. 2023

Microbiol Spectr

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FAM171B stabilizes vimentin and enhances CCL2-mediated TAM infiltration to promote bladder cancer progression

Hu,

Li,

Ning

et al. 2023

J Exp Clin Cancer Res

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Background Invasion and metastasis are the main causes of unfavourable prognosis in patients diagnosed with bladder cancer. The efficacy of immunotherapy in bladder cancer remains suboptimal due to the presence of an immunosuppressive microenvironment. The novel protein family with sequence similarity 171B (FAM171B) has been identified, but its precise role and mechanism in bladder cancer remain unclear. Methods In this study, we conducted an analysis to investigate the associations between FAM171B expression and the prognosis and clinicopathological stage of bladder cancer. To this end, we utilized RNA sequencing data from the TCGA and GEO databases, as well as tumor tissue specimens obtained from our clinical centre. RNA sequencing analysis allowed us to examine the biological function of FAM171B at the transcriptional level in bladder cancer cells. Additionally, we used immunoprecipitation and mass spectrometry to identify the protein that interacts with FAM171B in bladder cancer cells. The effects of FAM171B on modulating tumor-associated macrophages (TAMs) and vimentin-mediated tumor progression, as well as the underlying mechanisms, were clarified by phalloidin staining, immunofluorescence staining, ELISA, RNA immunoprecipitation, flow cytometry and a bladder cancer graft model. Results FAM171B expression exhibits strong positive correlation with poor survival outcomes and advanced clinicopathological stages in patients with bladder cancer. FAM171B significantly promoted bladder cancer growth and metastasis, accompanied by TAM accumulation in the microenvironment, in vivo and in vitro. Through studies of the molecular mechanism, we found that FAM171B contributes to tumor progression by stabilizing vimentin in the cytoplasm. Additionally, our research revealed that FAM171B enhances the splicing of CCL2 mRNA by interacting with heterogeneous nuclear ribonucleoprotein U (HNRNPU), ultimately leading to increased recruitment and M2 polarization of TAMs. Conclusions In this study, we identified FAM171B as a potent factor that promotes the progression of bladder cancer. These findings establish a solid theoretical foundation for considering FAM171B as a potential diagnostic and therapeutic biomarker for bladder cancer.

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LINC01559 promotes lung adenocarcinoma metastasis by disrupting the ubiquitination of VIM

Feng,

Cui,

Jiang

et al. 2023

Preprint

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Background: As the predominant proportion of lung cancer, lung adenocarcinoma (LUAD) has emerged as a formidable malignancy that poses a substantial menace to human health. Numerous studies have demonstrated the undeniable involvement of long non-coding RNAs (lncRNAs) in tumorigenesis and tumor progression. Our investigation aims to elucidate the functional role and intrinsic molecular mechanism of LINC01559 in LUAD metastasis. Methods: The expression and prognosis of LINC01559 in LUAD were analyzed from the database. Quantitative real‐time PCR (qRT-PCR) and In Situ Hybridization (ISH) were performed to detect the expression level of LINC01559 in LUAD cell lines and tissues. With RNA interference (RNAi) technology, the biological function of LINC01559 in LUAD cell lines was clarified through transwell assay. Tail vein injection model was established to observe the effect of LINC01559 on LUAD metastasis in vivo. RNA pull down and RNA immunoprecipitation (RIP) were utilized to explore the binding proteins of LINC01559. The rescue experiment was conducted to investigate the role of LINC01559 in promoting LUAD metastasis through vimentin (VIM). The molecular mechanism underlying the regulation of VIM by LINC01559 was elucidated using CHX-chase and ubiquitination assays. Results: LINC01559 exhibited conspicuous upregulation in both LUAD tissues and cell lines, and was identified as a prognostic risk factor for patients with LUAD. Notably, knockdown of LINC01559 expression significantly inhibited the migration and invasion capabilities of LUAD cells. In vivo assay revealed that knockdown of LINC01559 curbed lung metastasis of LUAD. Molecular mechanism studies unveiled that LINC01559 interacted with VIM and modulated its protein level. Further investigations suggested that LINC01559 promoted LUAD metastasis by impeding the ubiquitination-mediated degradation of VIM. Conclusions: Our results demonstrated that LINC01559 played a crucial role in fostering LUAD metastasis by stabilizing the VIM protein, which suggested that LINC01559 might be a potential therapeutic target for inhibiting LUAD metastasis.

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Vimentin epigenetic deregulation in Bladder Cancer associates with acquisition of invasive and metastatic phenotype through epithelial-to-mesenchymal transition

Cited by 6 publications

References 47 publications

Landscape of Exhausted T Cells in Tuberculosis Revealed by Single-Cell Sequencing

Landscape of Exhausted T Cells in Tuberculosis Revealed by Single-Cell Sequencing

FAM171B stabilizes vimentin and enhances CCL2-mediated TAM infiltration to promote bladder cancer progression

LINC01559 promotes lung adenocarcinoma metastasis by disrupting the ubiquitination of VIM

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