The long non-coding RNA PARROT is an upstream regulator of c-Myc and affects proliferation and translation

Vučićević, Dubravka; Gehre, Maja; Dhamija, Sonam; Friis‐Hansen, Lennart; Meierhofer, David; Sauer, Sascha; Ørom, Ulf Andersson

doi:10.18632/oncotarget.8985

Cited by 6 publications

(4 citation statements)

References 56 publications

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“…Among them, long noncoding RNAs (lncRNAs) have been widely implicated in post-transcriptional gene expression regulation. The expression level of lncRNAs is usually very low and tissue-specific[ 121 ]. c-MYC can regulate the expression of lncRNAs, some of these may also contribute to the transcription of c-MYC target genes[ 122 ].…”

Section: Anti-cancer Therapeutic Aspects Of C-myc In the Colonmentioning

confidence: 99%

“…PARROT has been also identified as an upstream regulator of c-MYC. Its depletion results in the depletion of c-MYC mRNA and protein expression, subsequently altering cell growth and proliferation[ 121 ]. In gastric cancer c-MYC activates the expression of colon cancer associated transcript 1 (CCAT1) lncRNA, leading to an increased proliferation and migration of cancer cells[ 123 ].…”

Section: Anti-cancer Therapeutic Aspects Of C-myc In the Colonmentioning

confidence: 99%

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Therapeutic aspects of c-MYC signaling in inflammatory and cancerous colonic diseases

Sípos¹,

Firneisz²,

Műzes³

2016

WJG

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Colonic inflammation is required to heal infections, wounds, and maintain tissue homeostasis. As the seventh hallmark of cancer, however, it may affect all phases of tumor development, including tumor initiation, promotion, invasion and metastatic dissemination, and also evasion immune surveillance. Inflammation acts as a cellular stressor and may trigger DNA damage or genetic instability, and, further, chronic inflammation can provoke genetic mutations and epigenetic mechanisms that promote malignant cell transformation. Both sporadical and colitis-associated colorectal carcinogenesis are multi-step, complex processes arising from the uncontrolled proliferation and spreading of malignantly transformed cell clones with the obvious ability to evade the host’s protective immunity. In cells upon DNA damage several proto-oncogenes, including c-MYC are activated in parelell with the inactivation of tumor suppressor genes. The target genes of the c-MYC protein participate in different cellular functions, including cell cycle, survival, protein synthesis, cell adhesion, and micro-RNA expression. The transcriptional program regulated by c-MYC is context dependent, therefore the final cellular response to elevated c-MYC levels may range from increased proliferation to augmented apoptosis. Considering physiological intestinal homeostasis, c-MYC displays a fundamental role in the regulation of cell proliferation and crypt cell number. However, c-MYC gene is frequently deregulated in inflammation, and overexpressed in both sporadic and colitis-associated colon adenocarcinomas. Recent results demonstrated that endogenous c-MYC is essential for efficient induction of p53-dependent apoptosis following DNA damage, but c-MYC function is also involved in and regulated by autophagy-related mechanisms, while its expression is affected by DNA-methylation, or histone acetylation. Molecules directly targeting c-MYC, or agents acting on other genes involved in the c-MYC pathway could be selected for combined regiments. However, due to its context-dependent cellular function, it is clinically essential to consider which cytotoxic drugs are used in combination with c-MYC targeted agents in various tissues. Increasing our knowledge about MYC-dependent pathways might provide direction to novel anti-inflammatory and colorectal cancer therapies.

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Section: Anti-cancer Therapeutic Aspects Of C-myc In the Colonmentioning

confidence: 99%

Section: Anti-cancer Therapeutic Aspects Of C-myc In the Colonmentioning

confidence: 99%

Therapeutic aspects of c-MYC signaling in inflammatory and cancerous colonic diseases

Sípos¹,

Firneisz²,

Műzes³

2016

WJG

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“…Liu et al have indicated that miR-18b inhibits TGF-β1-induced HFSc differentiation into smooth muscle cells by targeting SMAD2, which provided novel insights into the regulatory mechanisms of TGF-β-induced differentiation of HFSc (31). In addition, the lncRNA PARROT is regarded as a regulator of c-Myc and upregulates proliferation and translation of human mammary epithelial cells (32). We reported that PlncRNA-1 transfection increased Wnt signaling pathway downstream effectors Axin2, CyclinD1 and Myc gene expression in HFSc compared to control.…”

Section: Discussionmentioning

confidence: 99%

LncRNA PlncRNA‑1 regulates proliferation and differentiation of hair follicle stem cells through TGF‑β1‑mediated Wnt/β‑catenin signal pathway

Bai

et al. 2017

Mol Med Report

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The present study demonstrated that hair follicle stem cells (HFSc) have multidirectional differentiation potential and participate in skin wound healing processes. Long non‑coding RNAs (lncRNAs) are defined as non‑protein coding transcripts longer than 200 nucleotides, which are important in the proliferation and differentiation of cells. The purpose of the present study was to investigate the role of PlncRNA‑1 in the proliferation and differentiation of HFSc. Results revealed that PlncRNA‑1, transforming growth factor (TGF)‑β1, Wnt and β‑catenin expression levels were significantly downregulated in HFSc. PlncRNA‑1 transfection promoted proliferation and differentiation of HFSc. TGF‑β1, Wnt and β‑catenin expression levels were upregulated in HFSc following transfection of PlncRNA‑1. Results demonstrated that TGF‑β1 inhibitor LY2109761 blocked proliferation and differentiation of HFSc promoted by PlncRNA‑1 transfection. In addition, TGF‑β1 inhibitor LY2109761 led to decreased Wnt and β‑catenin expression levels in HFSc. Furthermore, PlncRNA‑1 transfection stimulated the cell cycle of HFSc, whereas TGF‑β1 inhibitor LY2109761 inhibited the cell cycle of HFSc and decreased the acceleration of the cell cycle induced by PlncRNA‑1 transfection. In conclusion, these findings suggest that PlncRNA‑1 may promote proliferation and differentiation of HFSc through upregulation of TGF‑β1‑mediated Wnt/β‑catenin signaling pathway.

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“…Several lncRNA studies reported senescence-suppressing results connecting to c-Myc. LncRNA PARROT, an upstream modulator of c-Myc, is downregulated in the senescence of human mammary epithelial cells [137]. c-Myc may transcriptionally activate some lncRNAs, such as USP2-AS1, to inhibit senescence and improve the proliferation of lung cancer cells [138].…”

Section: Akt Effector (C-myc)-regulating Lncrnas and Cell Functionsmentioning

confidence: 99%

Long Noncoding RNAs and Circular RNAs Regulate AKT and Its Effectors to Control Cell Functions of Cancer Cells

Tang

Chuang

Shiau

et al. 2022

Cells

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AKT serine-threonine kinase (AKT) and its effectors are essential for maintaining cell proliferation, apoptosis, autophagy, endoplasmic reticulum (ER) stress, mitochondrial morphogenesis (fission/fusion), ferroptosis, necroptosis, DNA damage response (damage and repair), senescence, and migration of cancer cells. Several lncRNAs and circRNAs also regulate the expression of these functions by numerous pathways. However, the impact on cell functions by lncRNAs and circRNAs regulating AKT and its effectors is poorly understood. This review provides comprehensive information about the relationship of lncRNAs and circRNAs with AKT on the cell functions of cancer cells. the roles of several lncRNAs and circRNAs acting on AKT effectors, such as FOXO, mTORC1/2, S6K1/2, 4EBP1, SREBP, and HIF are explored. To further validate the relationship between AKT, AKT effectors, lncRNAs, and circRNAs, more predicted AKT- and AKT effector-targeting lncRNAs and circRNAs were retrieved from the LncTarD and circBase databases. Consistently, using an in-depth literature survey, these AKT- and AKT effector-targeting database lncRNAs and circRNAs were related to cell functions. Therefore, some lncRNAs and circRNAs can regulate several cell functions through modulating AKT and AKT effectors. This review provides insights into a comprehensive network of AKT and AKT effectors connecting to lncRNAs and circRNAs in the regulation of cancer cell functions.

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The long non-coding RNA PARROT is an upstream regulator of c-Myc and affects proliferation and translation

Abstract: AbstrAct

Cited by 6 publications

References 56 publications

Therapeutic aspects of c-MYC signaling in inflammatory and cancerous colonic diseases

Therapeutic aspects of c-MYC signaling in inflammatory and cancerous colonic diseases

LncRNA PlncRNA‑1 regulates proliferation and differentiation of hair follicle stem cells through TGF‑β1‑mediated Wnt/β‑catenin signal pathway

Long Noncoding RNAs and Circular RNAs Regulate AKT and Its Effectors to Control Cell Functions of Cancer Cells

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