Circular RNA 100146 functions as an oncogene through direct binding to miR-361-3p and miR-615-5p in non-small cell lung cancer

Chen, Lijian; Nan, Aruo; Zhang, Nan; Jia, Yangyang; Li, Xin; Ling, Yihui; Dai, Jiabin; Zhang, Shaozhu; Yang, Qiaoyuan; Yi, Yanni; Jiang, Yanni

doi:10.1186/s12943-019-0943-0

Cited by 197 publications

(143 citation statements)

References 9 publications

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“…The previous study showed that hsa_circ_0062389 was one of the most upregulated circRNAs in NSCLC tissues [14] . However, the roles of hsa_circ_0062389 were still unclear.…”

Section: Hsa_circ_0062389 Was Up-regulated In Nsclcmentioning

confidence: 98%

hsa_circ_0062389 promotes the progression of non-small cell lung cancer by sponging miR-103a-3p to mediate CCNE1 expression

et al. 2020

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hsa_circ_0062389 miR-103a-3p CCNE1 Non-small cell lung cancer a b s t r a c tRecently, increasing evidence showed that circular RNAs (circRNAs) play critical roles in tumor progression. However, the roles of hsa_circ_0062389 in non-small cell lung cancer (NSCLC) development remain unclear. In the present study, hsa_circ_0062389 expression was significantly increased in NSCLC tissues and cell lines. High hsa_circ_0062389 expression was associated with advanced TNM stage and lymphnode metastasis. Function assays showed that hsa_circ_0062389 suppression reduced NSCLC cells proliferation and arrested cell cycle in G0/G1 phase. In mechanism, hsa_circ_0062389 directly interacted with miR-103a-3p in NSCLC, and CCNE1 acted as a target of miR-103a-3p. Furthermore, rescue assays showed that miR-103a-3p suppression or CCNE1 overexpression abolished the effects of hsa_circ_0062389 suppression on lung cancer cells progression. Therefore, our results showed that the hsa_circ_0062389/miR-103a-3p/CCNE1 axis might contribute to the tumorigenesis of NSCLC, which provided a new strategy for cancer treatment.

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“…The previous study showed that hsa_circ_0062389 was one of the most upregulated circRNAs in NSCLC tissues [14] . However, the roles of hsa_circ_0062389 were still unclear.…”

Section: Hsa_circ_0062389 Was Up-regulated In Nsclcmentioning

confidence: 98%

hsa_circ_0062389 promotes the progression of non-small cell lung cancer by sponging miR-103a-3p to mediate CCNE1 expression

et al. 2020

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“…Chen et al . found that the oncogene circRNA 100 146 promoted cell progression of NSCLC by targeting miR‐361‐3p . However, the mechanism of SNHG1 regulating miR‐361‐3p in NSCLC remains unclear.…”

Section: Introductionmentioning

confidence: 99%

LncRNA SNHG1 influences cell proliferation, migration, invasion, and apoptosis of non‐small cell lung cancer cells via the miR‐361‐3p/FRAT1 axis

Zheng

2019

Thoracic Cancer

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Background: Non-small-cell lung cancer (NSCLC) is the most lethal type of cancer. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been identified as crucial regulators in the development of NSCLC. The aim of our study was to explore the molecular mechanism of SNHG1 to enable better treatment for NSCLC patients. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the expression of Small nucleolar RNA host gene 1 (SNHG1), miR-361-3p and frequently rearranged in advanced T-cell lymphomas 1 (FRAT1). The protein level of FRAT1 was measured by western blot assay. Cell proliferation was evaluated by methyl thiazolyl tetrazolium (MTT) assay. Cell apoptosis was assessed by flow cytometry assay. The number of migrated and invaded cells were counted by transwell assay. The relationship between miR-361-3p and SNHG1 or FRAT1 was confirmed by dual-luciferase reporter assay. Results: Our results indicated that SNHG1 and FRAT1 were highly expressed in NSCLC tissues and cells. SNHG1 silencing inhibited proliferation, induced apoptosis and blocked migration and invasion of NSCLC cells. Also, FRAT1 downregulation suppressed proliferation, promoted apoptosis and hindered migration and invasion of NSCLC cells. Further, FRAT1 could recover the effects of SNHG1 silencing on proliferation, apoptosis, migration and invasion of NSCLC cells. SNHG1 sponged miR-361-3p and negatively regulated miR-361-3p expression. Meanwhile, miR-361-3p targeted FRAT1 and inversely modulated FRAT1 expression. In addition, miR-361-3p inhibition abated the effect of SNHG1 knockdown on FRAT1 expression. Conclusion: In conclusion, LncRNA SNHG1 promoted the proliferation, repressed apoptosis and enhanced migration and invasion of NSCLC cells by regulating FRAT1 expression via sponging miR-361-3p.

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“…Ren et al, 2019; Wei et al, 2019). Up to now, dozens of NSCLC-related circRNAs were screened and identified, such as circ_100146, CIRC-PRMT5 and circ_0026134 (Chang et al, 2019; L. Chen et al, 2019; Y.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies stated that circRNAs played vital roles in the development of NSCLC. For example, circ_100146 functioned as an oncogene, and its suppression hindered cell proliferation and invasion (L. Chen et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Circ_0005962 functions as an oncogene to aggravate non-small cell lung cancer progression via circ_0005962/miR-382-5p/PDK4 regulatory network

Zhenxiu¹,

Chen²,

Peng³

et al. 2020

Preprint

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Non-small cell lung cancer (NSCLC) is a leading threat to human lives with high incidence and mortality. Circular RNAs (circRNAs) were reported to play important roles in human cancers. The purpose of this study was to investigate the role of circ_0005962 and explore the underlying functional mechanisms. The expression of circ_0005962, miR-382-5p and pyruvate dehydrogenase kinase 4 (PDK4) was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation and cell apoptosis were assessed by cell counting kit-8 (CCK-8) assay and flow cytometry assay, respectively. The protein levels of Beclin 1, light chain3 (LC3-II/LC3-I), PDK4, Cleaved Caspase 3 (C-caspase 3) and proliferating cell nuclear antigen (PCNA) were examined using western blot analysis. Glycolysis was determined according to the levels of glucose consumption and lactate production. The interaction between miR-382-5p and circ_0005962 or PDK4 was predicted by the online tool CircInteractome or starbase and verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Xenograft model was constructed to investigate the role of circ_0005962 in vivo. circ_0005962 expressed with a high level in NSCLC tissues and cells. Circ_0005962 knockdown inhibited proliferation, autophagy, and glycolysis but promoted apoptosis in NSCLC cells. MiR-382-5p was targeted by circ_0005962, and its inhibition reversed the role of circ_0005962 knockdown. Besides, PDK4, a target of miR-382-5p, was regulated by circ_0005962 through miR-382-5p, and its overexpression abolished the effects of miR-382-5p reintroduction. Circ_0005962 knockdown suppressed tumor growth in vivo. Circ_0005962 knockdown restrained cell proliferation, autophagy, and glycolysis but stimulated apoptosis through modulating the circ_0005962/miR-382-5p/PDK4 axis. Our study broadened the insights into understanding the mechanism of NSCLC progression.

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Circular RNA 100146 functions as an oncogene through direct binding to miR-361-3p and miR-615-5p in non-small cell lung cancer

Cited by 197 publications

References 9 publications

hsa_circ_0062389 promotes the progression of non-small cell lung cancer by sponging miR-103a-3p to mediate CCNE1 expression

hsa_circ_0062389 promotes the progression of non-small cell lung cancer by sponging miR-103a-3p to mediate CCNE1 expression

LncRNA SNHG1 influences cell proliferation, migration, invasion, and apoptosis of non‐small cell lung cancer cells via the miR‐361‐3p/FRAT1 axis

Circ_0005962 functions as an oncogene to aggravate non-small cell lung cancer progression via circ_0005962/miR-382-5p/PDK4 regulatory network

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