α1,3-Fucosyltransferase-IX, an enzyme of pulmonary endogenous lung stem cell marker SSEA-1, alleviates experimental bronchopulmonary dysplasia

Chaubey, Sushma; Nader, Yaldah Mohammad; Shah, Dilip; Kumova, Ogan K.; Prahaladan, Varsha; Carey, Alison J.; Andersson, Sture; Bhandari, Vineet

doi:10.1038/s41390-020-0891-9

Cited by 6 publications

(5 citation statements)

References 44 publications

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“…In addition, the transcript levels of the FUT9 gene encoding a fucosyltransferase have been associated with the modulation of the immune response to pathogens [88] and the progression to apoptosis [89]. Remarkably, it has been shown that the intraperitoneal administration of FUT9 in neonatal mice alleviates experimental bronchopulmonary dysplasia, resulting in significant decrease in inflammation, alveolar-capillary leakage, alveolar simplification, and cell death [90].…”

Section: Discussionmentioning

confidence: 99%

Novel SARS-CoV-2 encoded small RNAs in the passage to humans

et al. 2020

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Motivation The Severe Acute Respiratory Syndrome-Coronavirus 2 (SARS-CoV-2) has recently emerged as the responsible for the pandemic outbreak of the coronavirus disease (COVID-19). This virus is closely related to coronaviruses infecting bats and Malayan pangolins, species suspected to be an intermediate host in the passage to humans. Several genomic mutations affecting viral proteins have been identified, contributing to the understanding of the recent animal-to-human transmission. However, the capacity of SARS-CoV-2 to encode functional putative microRNAs (miRNAs) remains largely unexplored. Results We have used deep learning to discover 12 candidate stem-loop structures hidden in the viral protein-coding genome. Among the precursors, the expression of eight mature miRNAs-like sequences was confirmed in small RNA-seq data from SARS-CoV-2 infected human cells. Predicted miRNAs are likely to target a subset of human genes of which 109 are transcriptionally deregulated upon infection. Remarkably, 28 of those genes potentially targeted by SARS-CoV-2 miRNAs are down-regulated in infected human cells. Interestingly, most of them have been related to respiratory diseases and viral infection, including several afflictions previously associated with SARS-CoV-1 and SARS-CoV-2. The comparison of SARS-CoV-2 pre-miRNA sequences with those from bat and pangolin coronaviruses suggests that single nucleotide mutations could have helped its progenitors jumping inter-species boundaries, allowing the gain of novel mature miRNAs targeting human mRNAs. Our results suggest that the recent acquisition of novel miRNAs-like sequences in the SARS-CoV-2 genome may have contributed to modulate the transcriptional reprogramming of the new host upon infection.

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Section: Discussionmentioning

confidence: 99%

Novel SARS-CoV-2 encoded small RNAs in the passage to humans

et al. 2020

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“…6E ). Molecules known to promote [ Il1a , Il1b , Il6 , Tnf , Nos2 , Cxcl5 , Mep1b, and Reg3b ( 57–62 )] and reduce [ Fut9 and Bpifb1 ( 63, 64 )] inflammation were increased and decreased, respectively in Filip1l -knockdown tumors ( Fig. 6E ).…”

Section: Resultsmentioning

confidence: 99%

Smoking-associated Downregulation of FILIP1L Enhances Lung Adenocarcinoma Progression Through Mucin Production, Inflammation, and Fibrosis

Kwon

Rubio

Wang

et al. 2022

Cancer Research Communications

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Lung adenocarcinoma (LUAD) is the major subtype in lung cancer, and cigarette smoking is essentially linked to its pathogenesis. We show that down-regulation of Filamin A interacting protein 1-like (FILIP1L) is a driver of LUAD progression. Cigarette smoking causes its down-regulation by promoter methylation in LUAD. Loss of FILIP1L increases xenograft growth, and, in lung-specific knockout mice, induces lung adenoma formation and mucin secretion. In syngeneic allograft tumors, reduction of FILIP1L and subsequent increase in its binding partner, prefoldin 1 (PFDN1) increases mucin secretion, proliferation, inflammation and fibrosis. Importantly, from the RNA-Seq analysis of these tumors, reduction of FILIP1L is associated with up-regulated Wnt/β-catenin signaling, which has been implicated in proliferation of cancer cells as well as inflammation and fibrosis within the tumor microenvironment. Overall, these findings suggest that down-regulation of FILIP1L is clinically relevant in LUAD, and warrant further efforts to evaluate pharmacologic regimens that either directly or indirectly restore FILIP1L-mediated gene regulation for the treatment of these neoplasms.

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“…These results suggested that SSEA-1 played a role in embryonic and tissue stem/progenitor cell maintenance. Furthermore, administration of Fut9 had increased SSEA-1 expression and cell proliferation resulting in the reverses of hyperoxia-induced cell death, airway inflammation, and lung injury in the murine model of neonatal bronchopulmonary dysplasia, suggesting the roles of SSEA-1 in immunomodulation and tissue regeneration ( Chaubey et al., 2021 ). Studies also suggested that SSEA-1 is an active modulator of Notch signaling for cell proliferation ( Yagi et al., 2012 ; Chaubey et al., 2021 ).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, administration of Fut9 had increased SSEA-1 expression and cell proliferation resulting in the reverses of hyperoxia-induced cell death, airway inflammation, and lung injury in the murine model of neonatal bronchopulmonary dysplasia, suggesting the roles of SSEA-1 in immunomodulation and tissue regeneration ( Chaubey et al., 2021 ). Studies also suggested that SSEA-1 is an active modulator of Notch signaling for cell proliferation ( Yagi et al., 2012 ; Chaubey et al., 2021 ). Notch signaling plays a crucial role in pulmonary development and regeneration, including cell fate determination, cell proliferation, and apoptosis ( Giuranno et al., 2019 ).…”

Section: Discussionmentioning

confidence: 99%