piR-36249 and DHX36 together inhibit testicular cancer cells progression by upregulating OAS2

Wang, Qianqian; Chen, Peize; Wang, Xiaorong; Wu, Yueming; Xia, Kaiguo; Mu, Xiangyu; Xuan, Qiang; Xiao, Jun; He, Yaohui; Li, Wen; Song, Xiaoyuan; Sun, Fei

doi:10.1016/j.ncrna.2022.12.004

Cited by 6 publications

(6 citation statements)

References 62 publications

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“…Examples include IFI27, IFI44L, IFIT1, OAS1, and OAS2. Notably, each of these genes has been associated with the promotion of cancer cell apoptosis [48][49][50][51][52]. In both of these cell lines, 4-5% of the total DEGs were included in this category.…”

Section: Selective Induction Of Degs Associated With Interferon Respo...mentioning

confidence: 99%

Dpep Inhibits Cancer Cell Growth and Survival via Shared and Context-Dependent Transcriptome Perturbations

Zhou,

Greene

2023

Cancers

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Dpep is a cell-penetrating peptide targeting transcription factors ATF5, CEBPB, and CEBPD, and that selectively promotes the apoptotic death of multiple tumor cell types in vitro and in vivo. As such, it is a potential therapeutic. To better understand its mechanism of action, we used PLATE-seq to compare the transcriptomes of six cancer cell lines of diverse origins before and after Dpep exposure. This revealed a context-dependent pattern of regulated genes that was unique to each line, but that exhibited a number of elements that were shared with other lines. This included the upregulation of pro-apoptotic genes and tumor suppressors as well as the enrichment of genes associated with responses to hypoxia and interferons. Downregulated transcripts included oncogenes and dependency genes, as well as enriched genes associated with different phases of the cell cycle and with DNA repair. In each case, such changes have the potential to lie upstream of apoptotic cell death. We also detected the regulation of unique as well as shared sets of transcription factors in each line, suggesting that Dpep may initiate a cascade of transcriptional responses that culminate in cancer cell death. Such death thus appears to reflect context-dependent, yet shared, disruption of multiple cellular pathways as well as of individual survival-relevant genes.

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Section: Selective Induction Of Degs Associated With Interferon Respo...mentioning

confidence: 99%

Dpep Inhibits Cancer Cell Growth and Survival via Shared and Context-Dependent Transcriptome Perturbations

Zhou,

Greene

2023

Cancers

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“…I have read the manuscript by Wang et al recently published in Noncoding RNA Research , suggesting that the piR-36249/DHX36/OAS2 axis regulates testicular cancer progression [ 1 ]. While the paper includes several interesting experiments, I am afraid it is affected by the PIWI-interacting RNA (piRNA) annotation problem that is widespread in the mammalian somatic piRNA literature [ 2 , 3 ].…”

mentioning

confidence: 99%

“…piR-36249 (DQ598183) is a tRNA-Cys 5’ half. The same genomic region in chromosome 17 that is shown in Wang et al [ 1 ] as the loci producing piR-36249 is annotated in the UCSC Genome Browser as tRNA-Cys, anticodon GCA (see HUGO or RepeatMasker tracks). Consistently, the sequence of piR-36249 is identical to the first 30 nucleotides of tRNA-Cys-GCA-2 based on the genomic tRNA database ( http://gtrnadb.ucsc.edu/ ).…”

mentioning

confidence: 99%

“…Additionally, while the biotinylated piR-36249 probe used for pull-down experiments contained the 5’ TOG motif, the control probe did not. It is therefore not surprising that DHX36 was experimentally identified as a piR-36249 interactor [ 1 ], because DHX36 binds G-quadruplexes with extremely high affinity [ 8 ].…”

mentioning

confidence: 99%

“…In their conclusion, Wang et al state that their data supports piR-36249 as a novel therapeutic target in testicular cancer [ 1 ]. However, targeting a tRNA gene would probably be toxic.…”

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confidence: 99%

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Letter to editor regarding “piR-36249 and DHX36 together inhibit testicular cancer cells progression by upregulating OAS2”

Tosar

2023

Non-coding RNA Research

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AT1R autoantibody promotes phenotypic transition of smooth muscle cells by activating AT1R-OAS2

Zhang,

Li,

Yan

et al. 2024

Biochemical Pharmacology

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piR-36249 and DHX36 together inhibit testicular cancer cells progression by upregulating OAS2

Cited by 6 publications

References 62 publications

Dpep Inhibits Cancer Cell Growth and Survival via Shared and Context-Dependent Transcriptome Perturbations

Dpep Inhibits Cancer Cell Growth and Survival via Shared and Context-Dependent Transcriptome Perturbations

Letter to editor regarding “piR-36249 and DHX36 together inhibit testicular cancer cells progression by upregulating OAS2”

AT1R autoantibody promotes phenotypic transition of smooth muscle cells by activating AT1R-OAS2

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