MicroRNA‐493‐5p‐mediated repression of the <i>MYCN</i> oncogene inhibits hepatic cancer cell growth and invasion

Yasukawa, Ken; Liew, Lee Chuen; Hagiwara, Kenta; Hironaka-Mitsuhashi, Ai; Qin, Xian; Furutani, Yutaka; Tanaka, Yasuhito; Nakagama, Hitoshi; Kato, Takashi; Ochiya, Takahiro; Gailhouste, Luc

doi:10.1111/cas.14292

Cited by 27 publications

(17 citation statements)

References 43 publications

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“…More and more evidence show that miRNAs play important roles in regulating cancer initiation and development ( Calin and Croce, 2006 ; Moles, 2017 ). Besides, miRNAs are critical for tumorigenesis and have been characterized as oncogenes or tumor suppressors ( Li et al, 2017 ; Xiao et al, 2019 ; Yasukawa et al, 2019 ; Zhang et al, 2019 ; Weidle et al, 2020 ). Yet the role of let-7a-5p in NSCLC has not been completely investigated.…”

Section: Introductionmentioning

confidence: 99%

Tanshinone Inhibits NSCLC by Downregulating AURKA Through Let-7a-5p

et al. 2020

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Lung cancer is the most deadly malignancy in the last decade, accounting for about 1.6 million deaths every year globally. Tanshinone is the constituent of Salvia miltiorrhiza; it has been found that they influence tumorigenesis. However, the role of tanshinones on lung cancer is still not clear. Let-7a-5p, a short non-coding RNA, is regarded as a suppressor gene in tumorigenesis. Herein, we verified that let-7a-5p is significantly downregulated in non-small-cell lung cancer (NSCLC) tissues and cell lines. Tanshinone suppressed the expression of aurora kinase A (AURKA), inhibited cell proliferation, and arrested cell cycle progression. Our results showed that tanshinones suppressed NSCLC by upregulating the expressions of let-7a-5p via directly targeting AURKA. Besides, the data reveal that the knockdown of AURKA can also inhibit cell proliferation, arrest cell cycle, and promote cell apoptosis. Furthermore, this study demonstrates that AURKA was negatively correlated with let-7a-5p in NSCLC patient tissues. Taken together, our findings suggest that tanshinone inhibits NSCLC by downregulating AURKA through let-7a-5p. Tanshinones and let-7a-5p have the potential to be candidates for drug development of NSCLC. In conclusion, this study revealed that tanshinones with miRNA linking lead to partial mechanism in NSCLC.

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Section: Introductionmentioning

confidence: 99%

Tanshinone Inhibits NSCLC by Downregulating AURKA Through Let-7a-5p

et al. 2020

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“…The MYCN oncogene is amplified in approximately 20% of neuroblastomas (NBs) ( 20 ). MYCN belongs to the Myc/Max/Mad/Mnt network of proteins that regulate proliferation, apoptosis, and differentiation ( 21 ), which were amplified in neuroblastoma, small-cell lung cancer ( 22 ) and hepatic cancer ( 23 ), respectively.…”

Section: Introductionmentioning

confidence: 99%

Copy Number Analysis Reveal Genetic Risks of Penile Cancer

Gao

Chen

et al. 2020

Front. Oncol.

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ObjectivesTo evaluate copy number alterations (CNAs) in genes associated with penile cancer (PeC) and determine their correlation and prognostic ability with PeC.MethodsWhole-exome sequencing was performed for tumor tissue and matched normal DNA of 35 patients diagnosed with penile squamous cell carcinoma from 2011 to 2016. Somatic CNAs were detected using the Genome Analysis Toolkit (GATK). Retrospective clinical data were collected and analyzed. All the data were statistically analyzed using SPSS 16.0 software. The cancer-specific survival rates were estimated by Kaplan-Meier curves and compared with the log-rank test.ResultsCNAs in the MYCN gene was detected in 19 (amplification: 54.29%) patients. Other CNAs gene targets were FAK (amplification: 45.72%, deletion: 8.57%), TP53 (amplification: 2.86%, deletion: 51.43%), TRKA (amplification: 34.29%, deletion: 2.86%), p75NTR (amplification: 5.71%, deletion: 42.86%), Miz-1 (amplification: 14.29%, deletion: 20.00%), Max (amplification: 17.14%, deletion: 2.86%), Bmi1 (amplification:14.29%, deletion: 48.57%), and MDM2 (amplification: 5.71%, deletion: 45.72%). The CNAs in MYCN and FAK correlated significantly with patient prognosis (P<0.05). The 3-year Recurrence-free survival rate was 87.10% among patients followed up. The 5-year survival rate of patients with MYCN amplification was 69.2%, compared to 94.4% in the non-amplification group. The 5-year survival rate of patients with FAK amplification was 65.6%, compared to 94.7% in the non-amplification group. The PPI network showed that TP53 and MYCN might play meaningful functional roles in PeC.ConclusionMYCN and FAK amplification and TP53 deletion were apparent in PeC. MYCN and TP53 were hub genes in PeC. MYCN and FAK amplification was also detected and analyzed, and the findings indicated that these two genes are predictors of poor prognosis in PeC.

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“…MicroRNAs (miRNAs) are a type of short non-coding RNAs with 21-25 nucleotides, acting as key players in the regulation of numerous tumors [18]. For example, miRNA-493-5p cuts down the expression of MYCN to repress cell growth and invasion in hepatic cancer [19]. MiR-324-5p inhibits cell metastasis in gallbladder carcinoma via downregulating TGFB2 [20].…”

Section: Discussionmentioning

confidence: 99%

LncRNA HOXA-AS2 Facilitates Cervical Cancer Progression and Angiogenesis via miR-509-3p/BTN3A1 Axis

Chen

2020

Preprint

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Background: Cervical cancer, the leading cause of cancer-relevant mortality in females, is an aggressive malignant tumor. Tumor angiogenesis is vital for cell proliferation and metastasis in cancers. Accumulating studies have claimed that long non-coding RNAs (lncRNAs) participate in the progression of various cancers. The aim of this research is to explore the biological role and regulatory mechanism of LncRNA HOXA-AS2 in cervical cancer.Methods: Experiments including RT-qPCR, western blot, RIP, MTT, EdU, transwell, luciferase reporter, RIP, FISH, tube formation assays were applied to investigate the biological role and regulatory mechanism of LncRNA HOXA-AS2 in cervical cancer.Results: In current study, the results disclosed that HOXA-AS2 was notably upregulated in cervical cancer tissues and cell lines, and high HOXA-AS2 expression was strongly associated with poor prognosis of cervical cancer patients. Furthermore, HOXA-AS2 contributed to cell proliferation, migration, invasion and angiogenesis in cervical cancer. In addition, HOXA-AS2 absorbed miR-509-3p and miR-509-3p targeted BTN3A1 in cervical cancer. Besides, BTN3A1 overexpression partly rescued the inhibitory influence of HOXA-AS2 knockdown on cervical cancer progression and angiogenesis. Overall, HOXA-AS2 promoted cervical cancer progression and angiogenesis through sponging miR-509-3p to elevate BTN3A1 expression. Conclusions: In other words, this paper was the first to study the molecular regulatory mechanism of HOXA-AS2 in cervical cancer and certified that HOXA-AS2 accelerated progression and angiogenesis in cervical cancer by targeting miR-509-3p/BTN3A1 axis, which may become a beneficial therapeutic target for cervical cancer.

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MicroRNA‐493‐5p‐mediated repression of the MYCN oncogene inhibits hepatic cancer cell growth and invasion

Cited by 27 publications

References 43 publications

Tanshinone Inhibits NSCLC by Downregulating AURKA Through Let-7a-5p

Tanshinone Inhibits NSCLC by Downregulating AURKA Through Let-7a-5p

Copy Number Analysis Reveal Genetic Risks of Penile Cancer

LncRNA HOXA-AS2 Facilitates Cervical Cancer Progression and Angiogenesis via miR-509-3p/BTN3A1 Axis

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