The Role of Non-Coding RNAs in the Regulation of the Proto-Oncogene MYC in Different Types of Cancer

Stasevich, Ekaterina Mikhailovna; Murashko, Matvey Mikhailovich; Zinevich, L. S.; Demin, D. E.; Schwartz, Anton M.

doi:10.3390/biomedicines9080921

Cited by 16 publications

(9 citation statements)

References 292 publications

(325 reference statements)

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“…Among various oncogenes, c-Myc, which is a strong transcription factor participating in several aspects of the oncogenic process, acts as a vital member of the Myc family ( 40 ). The idea that c-Myc serves an important role in cell proliferation and differentiation has been proposed and confirmed ( 41 ). The relevant protein encoded by c-Myc affects cell proliferation ( 42 ).…”

Section: Discussionmentioning

confidence: 92%

3‑Bromopyruvic acid regulates glucose metabolism by targeting the c‑Myc/TXNIP axis and induces mitochondria‑mediated apoptosis in TNBC cells

Pan

Liu

et al. 2022

Exp Ther Med

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Aerobic glycolysis is commonly observed in tumor cells, including triple-negative breast cancer (TNBC) cells, and the rate of aerobic glycolysis is higher in TNBC cells than in non-TNBC cells. Hexokinase 2 (HK2) is a key enzyme in the glycolytic pathway and a target of the transcription factor c-Myc, which is highly expressed in TNBC and promotes aerobic glycolysis by enhancing HK2 expression. As an inhibitor of HK2, 3-bromopyruvic acid (3-BrPA) exhibits good therapeutic efficacy in intrahepatic and extrahepatic tumors and inhibits the proliferation of human tumor cells with high expression levels of c-Myc in vivo and in vitro . In addition, 3-BrPA combines with photodynamic therapy to inhibit TNBC cell migration. Thioredoxin-interacting protein (TXNIP) competes with c-Myc to reduce glucose consumption in tumor cells to restrain cell proliferation. A comparative analysis was performed in the present study in TNBC (HCC1143) and non-TNBC (MCF-7) cell lines to explore the effect of 3-BrPA on energy metabolism in TNBC cells and to investigate the possible mechanism of action. Cell viability and apoptosis were detected through Cell Counting Kit-8 and flow cytometry assays, respectively. Expression levels of HK2, glucose transporter 1, TXNIP, c-Myc and mitochondria-regulated apoptosis pathway proteins were measured through western blotting. 3-BrPA inhibited cell proliferation, downregulated c-Myc and HK2 expression, and upregulated TXNIP expression in TNBC cells, but it doesn't have the same effect on non-TNBC cells. Furthermore, 3-BrPA induced the typical manifestations of mitochondrial-mediated apoptosis such as decreasing Bcl-2 expression and increasing Bax, Cyt-C and Caspase-3 expression. The present results suggested that 3-BrPA promoted TXNIP protein expression and reduced HK2 expression in TNBC cells by downregulating c-Myc expression, inhibiting glycolysis including suppressing lactate generation, intracellular ATP generation and HK activity, inducing mitochondrial-mediated apoptosis and eventually suppressing TNBC cell proliferation. These findings may reveal a novel therapeutic target for the clinical treatment of TNBC.

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Section: Discussionmentioning

confidence: 92%

3‑Bromopyruvic acid regulates glucose metabolism by targeting the c‑Myc/TXNIP axis and induces mitochondria‑mediated apoptosis in TNBC cells

Pan

Liu

et al. 2022

Exp Ther Med

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“…Importantly, this mode of antisense-mediated regulation doesn’t solely revolve around NAT6531. Another NAT known as NAT7281 plays a role in repressing c-MYC transcription [ 110 ]. It also plays a crucial part in silencing the expression of NAT6531 and the small RNAs it produces.…”

Section: Human Diseases and The Molecular Significance Of Natural Ant...mentioning

confidence: 99%

Therapeutic potential of natural antisense transcripts and various mechanisms involved for clinical applications and disease prevention

Ali,

Khatoon,

Shao

et al. 2023

RNA Biology

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Antisense transcription, a prevalent occurrence in mammalian genomes, gives rise to natural antisense transcripts (NATs) as RNA molecules. These NATs serve as agents of diverse transcriptional and post-transcriptional regulatory mechanisms, playing crucial roles in various biological processes vital for cell function and immune response. However, when their normal functions are disrupted, they can contribute to human diseases. This comprehensive review aims to establish the molecular foundation linking NATs to the development of disorders like cancer, neurodegenerative conditions, and cardiovascular ailments. Additionally, we evaluate the potential of oligonucleotide-based therapies targeting NATs, presenting both their advantages and limitations, while also highlighting the latest advancements in this promising realm of clinical investigation. Abbreviations: NATs- Natural antisense transcripts, PRC1- Polycomb Repressive Complex 1, PRC2- Polycomb Repressive Complex 2, ADARs- Adenosine deaminases acting on RNA, BDNF-AS- Brain-derived neurotrophic factor antisense transcript, ASOs- Antisense oligonucleotides, SINEUPs- Inverted SINEB2 sequence-mediated upregulating molecules, PTBP1- Polypyrimidine tract binding protein-1, HNRNPK- heterogeneous nuclear ribonucleoprotein K, MAPT-AS1- microtubule-associated protein tau antisense 1, KCNQ1OT- (KCNQ1 opposite strand/antisense transcript 1, ERK- extracellular signal-regulated kinase 1, USP14- ubiquitin-specific protease 14, EGF- Epidermal growth factor, LSD1- Lysine Specific Demethylase 1, ANRIL- Antisense Noncoding RNA in the INK4 Locus, BWS- Beckwith-Wiedemann syndrome, VEGFA- Vascular Endothelial Growth component A

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“…lncRNAs have emerged as crucial regulatory molecules [ 38 , 39 , 97 , 98 , 99 ]. In the last few years, an intricate network between MYC and lncRNAs has come into view; it presents many of the features of symbiotic relationships [ 48 , 52 , 100 , 101 ].…”

Section: Concluding Considerationsmentioning

confidence: 99%

“…They establish a link between MYC, lncRNA expression, and cell proliferation, raising the question of the role of the lncRNA–MYC network in cancer. This general question has been illuminated by several recent reviews [ 26 , 45 , 47 , 48 , 49 , 50 , 51 , 52 ].…”

Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNAs as “MYC Facilitators”

García-Caballero,

Hart,

Vogt

2023

Pathophysiology

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In this article, we discuss a class of MYC-interacting lncRNAs (long non-coding RNAs) that share the following criteria: They are direct transcriptional targets of MYC. Their expression is coordinated with the expression of MYC. They are required for sustained MYC-driven cell proliferation, and they are not essential for cell survival. We refer to these lncRNAs as “MYC facilitators” and discuss two representative members of this class of lncRNAs, SNHG17 (small nuclear RNA host gene) and LNROP (long non-coding regulator of POU2F2). We also present a general hypothesis on the role of lncRNAs in MYC-mediated transcriptional regulation.

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The Role of Non-Coding RNAs in the Regulation of the Proto-Oncogene MYC in Different Types of Cancer

Cited by 16 publications

References 292 publications

3‑Bromopyruvic acid regulates glucose metabolism by targeting the c‑Myc/TXNIP axis and induces mitochondria‑mediated apoptosis in TNBC cells

3‑Bromopyruvic acid regulates glucose metabolism by targeting the c‑Myc/TXNIP axis and induces mitochondria‑mediated apoptosis in TNBC cells

Therapeutic potential of natural antisense transcripts and various mechanisms involved for clinical applications and disease prevention

Long Non-Coding RNAs as “MYC Facilitators”

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