TNF-α differentially regulates cell cycle genes in promyelocytic and granulocytic HL-60/S4 cells

Jacobson, Elsie C.; Perry, Jo K.; Vickers, Mark H.; Olins, Ada L.; Olins, Donald E.; O’Sullivan, Justin M.

doi:10.1101/471789

Cited by 4 publications

(4 citation statements)

References 75 publications

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“…To see if we could identify common and additional SVs from RNA-seq we used STAR-fusion v1.4.0 [27] on the HL-60/CICLR and HL-60/S4 cell transcription profiles. We analyzed HL-60/S4 gene fusions in two RNA-seq experiments from two different laboratories [22,28]. We analyzed HL-60/CICLR gene fusions in one RNA-seq experiment [24], the same source that used to acquire Hi-C data.…”

Section: Structural Variants Detected With Hi-c and Rna-seqmentioning

confidence: 99%

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Hi-C detects novel structural variants in HL-60 and HL-60/S4 cell lines

et al. 2020

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Cancer cell lines often have large structural variants (SVs) that evolve over time. There are many reported differences in large scale SVs between HL-60 and HL-60/S4, two cell lines derived from the same acute myeloid leukemia sample. However, the stability and variability of inter-and intra-chromosomal structural variants between different sources of the same cell line is unknown. Here, we used Hi-C and RNA-seq to identify and compare large SVs in HL-60 and HL-60/S4 cell lines. Comparisons with previously published karyotypes identified novel SVs in both cell lines. Hi-C was used to characterize the known expansion centered on the MYC locus. The MYC expansion was integrated into known locations in HL-60/S4, and a novel location (chr4) in HL-60. The HL-60 cell line has more within-line structural variation than the HL-60/S4 derivative cell line. Collectively we demonstrate the usefulness of Hi-C and with RNA-seq data for the identification and characterization of SVs.

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Section: Structural Variants Detected With Hi-c and Rna-seqmentioning

confidence: 99%

“…We analyzed HL-60/CICLR gene fusions in one RNA-seq experiment [24], the same source that used to acquire Hi-C data. All experimental datasets [22,24,28] included both undifferentiated and granulocytic (i.e. ATRA-differentiated) cells.…”

Section: Structural Variants Detected With Hi-c and Rna-seqmentioning

confidence: 99%

Hi-C detects novel structural variants in HL-60 and HL-60/S4 cell lines

et al. 2020

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“…Further analysis of the RNA-seq data showed that genes closely related to the DNA damage repair (Bax, Bcl3, Brac1, Fignl1), DNA replication (Gins3, Mcm3), and cell cycle progression (Ccnb1, Cdk1, Cdc6, and Nek6) were significantly changed with additional hAECs or EXOs treatment (Table 1). TNF-α has been reported to regulate cell cycle progression in different types of cancer cells (Pusztai et al, 1993;Zhang et al, 2018;Jacobson et al, 2019). Recently, studies have shown that combination with low-dose TNF-α could enhance therapeutic effects of chemotherapeutic drugs through the TNF-α/NFκB signaling cascade, driving quiescent cancer cells out of G0/G1 phase to enter treatment sensitive proliferating phases to be killed by chemotherapeutic drugs (Moon et al, 2010;Jayasooriya et al, 2013;Wu et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Human Amniotic Epithelial Cells and Their Derived Exosomes Protect Against Cisplatin-Induced Acute Kidney Injury Without Compromising Its Antitumor Activity in Mice

Kang

Chen

Xin

et al. 2022

Front. Cell Dev. Biol.

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Background: Cisplatin is a widely used chemotherapeutic drug, whereas the clinical application is greatly limited by its nephrotoxic side effect. Currently, there has been no effective treatment to prevent cisplatin-induced acute kidney injury (cisplatin-AKI). Human amniotic epithelial cells (hAECs) and their derived exosomes (EXOs) have been proven to effectively protect against ischemia reperfusion-induced AKI, yet their roles in cisplatin-AKI are still unknown.Methods: C57BL/6J mice were given two doses of cisplatin at 20 or 15 mg/kg of body weight to induce AKI with or without mortality. hAECs or EXOs were injected via tail vein 1 day after cisplatin administration. Serum and kidney tissues were collected on the fourth day after 15 mg/kg cisplatin treatment to explore the nephro-protective effects of hAECs and EXOs on cisplatin-AKI. Lung cancer xenograft model was built by subcutaneous injection of A549 cells into BALB/c nude mice to evaluate the effect of hAECs or EXOs on cisplatin chemotherapy.Results: Cisplatin nephrotoxicity was significantly attenuated by hAECs and EXOs as evidenced by reduced mortality rate and decreased serum creatinine (sCr) and reduced tubular injury score. hAECs or EXOs exerted the nephro-protective effects via suppression of TNF-α/MAPK and caspase signaling pathways. In the A549 lung cancer xenograft mouse model, administration of hAECs or EXOs did not promote tumor growth or compromise the therapeutic effects of cisplatin on tumors.Conclusion: This study is the first to demonstrate that hAECs and their derived exosomes have nephro-protective effects in cisplatin-AKI in vivo. Importantly, neither hAECs nor EXOs compromise the antitumor activity of cisplatin. These results potentially support the use of hAECs and their derived EXOs as nephro-protectors against cisplatin-induced nephrotoxicity clinically.

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“…However, selective depletion of YTHDF2 inhibits the self-renewal capacity of leukemic cells and promotes cell-differentiation and apoptosis, suggesting the therapeutic value of YTHDF2 in controlling AML progression. Experimentally, they found that, YTHDF2 targets tumor necrosis factor-α (TNF-α), required for cell-necrosis and apoptosis [67], and inhibits its expression by m6A-mediated mRNA decay mechanism [38]. However, selective removal of YTHDF2 increased the expression of TNF-α by lowering mRNA decay, confirmed by increased half-life of the target mRNA, and thereby increased terminal cell differentiation and apoptosis.…”

Section: Alkbh5 In Amlmentioning

confidence: 99%

Immunotherapeutic Potential of m6A-Modifiers in Controlling Acute Myeloid Leukemia

Kumar¹,

Nagpal²,

Kumar³

et al. 2021

Preprint

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Epigenetic alterations have contributed greatly to human carcinogenesis. Conventional epigenetic studies have been predominantly focused on DNA methylation, histone modifications and chromatin remodelling. However, recently, RNA modification (m6A-methylation) also termed ‘epitranscriptomics’ has emerged as a new layer of epigenetic regulation due to its diverse role in various biological processes. In this review, we have summarized the therapeutic potential of m6A-modifiers in controlling haematological disorders especially acute myeloid leukemia (AML). It is a type of blood cancer affecting specific subsets of blood-forming hematopoietic stem/progenitor cells (HSPCs) which proliferate rapidly and acquire self-renewable capacities with impaired terminal cell-differentiation and apoptosis leading to abnormal accumulation of white blood cells, and thus an alternative therapeutic approach is required urgently. Here, we have described how RNA m6A-modification machineries EEE (Editor/writer: Mettl3, Mettl14; Eraser/remover: FTO, ALKBH5 and Effector/reader: YTHDF-1/2) could be reformed into potential druggable candidate or as RNA modifying drug (RMD) to treat leukemia. Moreover, we have shed-light on the role of microRNA and suppressor of cytokine signalling (SOCS/CISH) in increasing anti-tumor immunity towards leukemia. We anticipate, our investigation will provide a fundamental knowledge in nurturing the potential of RNA modifiers in discovering novel therapeutics or immunotherapeutic procedures.

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TNF-α differentially regulates cell cycle genes in promyelocytic and granulocytic HL-60/S4 cells

Cited by 4 publications

References 75 publications

Hi-C detects novel structural variants in HL-60 and HL-60/S4 cell lines

Hi-C detects novel structural variants in HL-60 and HL-60/S4 cell lines

Human Amniotic Epithelial Cells and Their Derived Exosomes Protect Against Cisplatin-Induced Acute Kidney Injury Without Compromising Its Antitumor Activity in Mice

Immunotherapeutic Potential of m6A-Modifiers in Controlling Acute Myeloid Leukemia

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