MYC modulators in cancer: a patent review

Wang, Xiaona; Su, Xiao-Xuan; Cheng, Sui-Qi; Sun, Zhongguo; Huang, Zhi‐Shu; Ou, Tian‐Miao

doi:10.1080/13543776.2019.1612878

Cited by 19 publications

(16 citation statements)

References 151 publications

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“…Altogether these data suggest that PNO1 may promote EC progression via upregulating NF-κB p65, CTNNB1, Twist, Myc and MMP2 expression. Our study was consistent with previous studies (27)(28)(29).…”

Section: Discussionsupporting

confidence: 94%

“…PNO1 was observed to promote EC metastasis in previous studies, and the expression levels of Twist, Myc and MMP2, which are genes known to participate in the tumor metastasis process (27)(28)(29), were also analyzed following the KD of PNO1. The results suggested that PNO1 may promote EC metastasis via upregulating Twist, Myc and MMP2 expression levels.…”

Section: Discussionmentioning

confidence: 99%

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Knockdown of PNO1 inhibits esophageal cancer progression

Wang

et al. 2021

Oncol Rep

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The present study aimed to investigate the role of partner of NOB1 homolog (PNO1) in esophageal cancer (EC). The expression levels of PNO1 in EC were primarily analyzed using data obtained from databases. PNO1 expression was also knocked down in EC cells (Eca-109 and TE1) to determine the biological effects of PNO1 on tumorigenesis in vitro and in vivo. In addition, possible downstream targets of PNO1 in EC were identified. The expression levels of PNO1 were upregulated in the tumor tissues compared with that noted in normal tissues. Moreover, the knockdown (KD) of PNO1 suppressed cell proliferation, migration and invasion, and promoted cell apoptosis (P<0.05). Furthermore, the protein expression levels of AKT1, Twist, Myc, mTOR, matrix metalloproteinase 2 (MMP2), nuclear factor (NF)-κB p65 and β-catenin 1 (CTNNB1) were downregulated following the KD of PNO1 in Eca-109 cells (P<0.05). In addition, the overexpression of CTNNB1 reversed the effects of PNO1 KD in Eca-109 cells (P<0.05). In conclusion, the findings of the present study suggest that PNO1 promotes EC progression by regulating AKT1, Twist, Myc, mTOR, MMP2, NF-κB p65 and CTNNB1 expression.Construction of stable PNO1-knockdown (KD) and β-catenin (CTNNB1)-overexpressing cells. PNO1 was stably knocked down in Eca-109 and TE-1 cells using short hairpin RNA (sh), and CTNNB1 was stably overexpressed in Eca-109 cells only. sh-PNO1-KD, sh-PNO1-negative control (NC), sh-CTNNB1-OE and sh-CTNNB1-negative control (NC)

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Knockdown of PNO1 inhibits esophageal cancer progression

Wang

et al. 2021

Oncol Rep

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“…Interestingly, one cluster associated with TBK1 did not appear in the higher threshold analysis and demonstrated a clear decrease in as a function of dose ( Figure S20). Lastly, a major oncogene MYC [68,69] did not show up in the higher threshold analysis, whereas in this analysis MYC was clearly being activated with increasing dose ( Figure S20), indicating that space radiation exposure would increase the potential for carcinogenesis.…”

Section: Gsea C6: Oncogenic Signaturesmentioning

confidence: 79%

NASA GeneLab Platform Utilized for Biological Response to Space Radiation in Animal Models

McDonald¹,

Stainforth

Cahill

et al. 2020

Cancers

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Background: Ionizing radiation from galactic cosmic rays (GCR) is one of the major risk factors that will impact the health of astronauts on extended missions outside the protective effects of the Earth’s magnetic field. The NASA GeneLab project has detailed information on radiation exposure using animal models with curated dosimetry information for spaceflight experiments. Methods: We analyzed multiple GeneLab omics datasets associated with both ground-based and spaceflight radiation studies that included in vivo and in vitro approaches. A range of ions from protons to iron particles with doses from 0.1 to 1.0 Gy for ground studies, as well as samples flown in low Earth orbit (LEO) with total doses of 1.0 mGy to 30 mGy, were utilized. Results: From this analysis, we were able to identify distinct biological signatures associating specific ions with specific biological responses due to radiation exposure in space. For example, we discovered changes in mitochondrial function, ribosomal assembly, and immune pathways as a function of dose. Conclusions: We provided a summary of how the GeneLab’s rich database of omics experiments with animal models can be used to generate novel hypotheses to better understand human health risks from GCR exposures.

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“…c-Myc is a well-known oncogene that activates a variety of oncogenic signaling pathways [24]. c-Myc is shown to be frequently overexpressed in multiple cancers, and its expression is tightly controlled by different factors at the transcription or post-transcription level [25]. Up to now, only a few studies focused the regulatory role of lncRNA on c-Myc mRNA stability.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: A novel positive feedback loop of linc02042 and c-Myc mediated by YBX1 promotes tumorigenesis and metastasis in esophageal squamous cell carcinoma

Zhang

Qiu

et al. 2020

Cancer Cell Int

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Background: Long non-coding RNA (lncRNA) is a class of endogenous RNA with a length of more than 200 nucleotides, which is emerging as a pivotal player in cancer development and progression. However, the functional roles of many members in this class remain largely uncharacterized. In the present study, we explored the biological relevance of linc02042 in esophageal squamous cell carcinoma (ESCC). Methods: qRT-PCR was used to detect the levels of linc02042 and c-Myc. Western blot was used to assess protein expression level. CCK-8 and Transwell assays were employed to test ESCC cell proliferation and invasion, respectively. The mice study including xenograft tumor and lung metastasis models was used to determine the role of linc02042 in vivo. RNA pull-down, ChIP and luciferase reporter assays were employed to test the relationship between linc02042, YBX1 and c-Myc. Results: Linc02042 was found to be markedly upregulated in ESCC cell lines, tissues and plasma, and was closely correlated with malignant clinical features. Knockdown of linc02042 significantly inhibited ESCC cell viability and invasion in vitro as well as tumor growth and lung metastasis in vivo, whereas overexpression of linc02042 resulted in the opposite results. Mechanistically, linc02042 acted as a scaffold for YBX-1 binding to the 3′-UTR of c-Myc mRNA, leading to enhanced c-Myc mRNA stability, thereby facilitating ESCC growth and metastasis. Moreover, in turn, c-Myc was able to transcriptionally elevate linc02042 by directly binding to the E-box motif proximal to the transcription start site (TSS) of linc02042 promoter. Clinically, linc02042 was identified as an effective diagnostic and prognostic biomarker for ESCC patients, and its expression was strongly positively correlated with c-Myc expression in ESCC tissues. Conclusion: Our data suggest that linc02042 plays an important tumor-promoting role in ESCC, which lays a foundation for considering it as a potential target for ESCC patients.

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MYC modulators in cancer: a patent review

Cited by 19 publications

References 151 publications

Knockdown of PNO1 inhibits esophageal cancer progression

Knockdown of PNO1 inhibits esophageal cancer progression

NASA GeneLab Platform Utilized for Biological Response to Space Radiation in Animal Models

RETRACTED ARTICLE: A novel positive feedback loop of linc02042 and c-Myc mediated by YBX1 promotes tumorigenesis and metastasis in esophageal squamous cell carcinoma

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