Circular RNA circPITX1 knockdown inhibits glycolysis to enhance radiosensitivity of glioma cells by miR-329-3p/NEK2 axis

Guan, Yongchang; Cao, Zhi; Du, Jinghua; Liu, Tao; Wang, Tingzhong

doi:10.1186/s12935-020-01169-z

Cited by 46 publications

(46 citation statements)

References 35 publications

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“…For instance, circPITX1 silencing elevated the radiosensitivity of glioma cells through suppressing the glycolysis by regulating miR-329-3p/NEK2 axis. 25 Loss-of-function experiments were employed to explore the functions of circ-ZNF609 in PCa cells. Circ-ZNF609 knockdown caused the suppression of the viability, migration and invasion and the promotion on the apoptosis of PCa cells.…”

Section: Discussionmentioning

confidence: 99%

<p>Circ-ZNF609 Accelerates the Radioresistance of Prostate Cancer Cells by Promoting the Glycolytic Metabolism Through miR-501-3p/HK2 Axis</p>

Zhang²,

Ren

et al. 2020

CMAR

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Background: The development of radioresistance remains the obstacle for prostate cancer (PCa) treatment. Here, we explored the role and potential mechanism of circular RNA zinc finger protein 609 (circ-ZNF609) in the radioresistance of PCa cells. Materials and Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of circ-ZNF609, microRNA-501-3p (miR-501-3p) and hexokinase 2 (HK2) messenger RNA (mRNA). The viability, apoptosis, metastasis and radioresistance of PCa cells were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry, transwell assays and colony formation assay. The glycolytic rate was assessed through measuring the glucose consumption and lactate production using fluorescencebased glucose and lactate assay kits. The target interaction between miR-501-3p and circ-ZNF609 or HK2 was predicted by StarBase software and confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. The protein level of HK2 was detected by Western blot assay. In vivo tumor growth assay was used to explore the role of circ-ZNF609 in the radioresistance of PCa in vivo. Results: Circ-ZNF609 was abnormally up-regulated in PCa tissues and cell lines. Circ-ZNF609 silencing hampered the viability, metastasis, radioresistance and promoted the apoptosis through suppressing cell glycolysis. MiR-501-3p was a direct target of circ-ZNF609, and si-circ-ZNF609-induced influence in PCa cells was partly alleviated by the addition of anti-miR-501-3p. MiR-501-3p functioned through directly interacting with and down-regulating HK2. HK2 was modulated by circ-ZNF609/miR-501-3p axis in PCa cells. Circ-ZNF609 silencing enhanced the radiosensitivity of PCa cells in vivo. Conclusion: Circ-ZNF609 promoted the progression and radioresistance of PCa cells through accelerating the glycolysis via miR-501-3p/HK2 axis, providing promising targets for improving the prognosis of PCa patients.

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Section: Discussionmentioning

confidence: 99%

<p>Circ-ZNF609 Accelerates the Radioresistance of Prostate Cancer Cells by Promoting the Glycolytic Metabolism Through miR-501-3p/HK2 Axis</p>

Zhang²,

Ren

et al. 2020

CMAR

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“…NEK2 is a poorly-characterized gene, encoding a serine/threonine kinase (32). Its elevated expression has been reported in various cancers including breast, lung, colorectal cancers and glioma (36)(37)(38)(39)(40). Higher expression of NEK2 is correlated with poorer prognosis of (which was not certified by peer review) is the author/funder.…”

Section: Discussionmentioning

confidence: 99%

Spatiotemporal Dynamics of Intra-tumoral Dependence on NEK2-EZH2 Signaling in Glioblastoma Cancer Progression

Wang

Pavliukov

Yamashita³

et al. 2020

Preprint

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The highly lethal brain cancer glioblastoma undergoes dynamic changes in molecular profile and cellular phenotype throughout tumor core establishment and in primary-to-recurrent tumor progression. These dynamic changes allow glioblastoma tumors to escape from multimodal therapies, resulting in patient lethality. Here, we identified the emergence of dependence on NEK2-mediated EZH2 signaling, specifically in therapy-resistant tumor core-located glioblastoma cells. In patient-derived glioblastoma core models, NEK2 was required for in vivo tumor initiation, propagation, and radio-resistance. Mechanistically, in glioblastoma core cells, NEK2 binds with EZH2 to prevent its proteasome-mediated degradation in a kinase-dependent manner. Clinically, NEK2 expression is elevated in recurrent tumors after therapeutic failure as opposed to their matched primary untreated cases, and its high expression is indicative of worse prognosis. For therapeutic development, we designed a novel NEK2 kinase inhibitor CMP3a, which effectively attenuated growth of murine glioblastoma models and exhibited a synergistic effect with radiation therapy. Collectively, the emerging NEK2-EZH2 signaling axis is critical in glioblastoma, particularly within the tumor core, and the small molecule inhibitor CMP3a for NEK2 is a potential novel therapeutic agent for glioblastoma.

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“…Similarly, circPITX1 was found to target miR-329-3p, which in turn targets a kinase involved in mitosis, Nek2. 79 In a glioma model, Guan et al demonstrated that by silencing circPITX1, its target miR-329-3p inhibited Nek2, resulting in repressed viability, glycolysis and colony formation and thus increased radiosensitivity. 79 Recently, Niu et al described the role of circTUBD1 in radiation-induced liver disease.…”

Section: Circrnas In Radiation Responsementioning

confidence: 99%

Long and short non-coding RNA and radiation response: a review

May

Bylicky

Chopra

et al. 2021

Translational Research

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This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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Circular RNA circPITX1 knockdown inhibits glycolysis to enhance radiosensitivity of glioma cells by miR-329-3p/NEK2 axis

Cited by 46 publications

References 35 publications

<p>Circ-ZNF609 Accelerates the Radioresistance of Prostate Cancer Cells by Promoting the Glycolytic Metabolism Through miR-501-3p/HK2 Axis</p>

<p>Circ-ZNF609 Accelerates the Radioresistance of Prostate Cancer Cells by Promoting the Glycolytic Metabolism Through miR-501-3p/HK2 Axis</p>

Spatiotemporal Dynamics of Intra-tumoral Dependence on NEK2-EZH2 Signaling in Glioblastoma Cancer Progression

Long and short non-coding RNA and radiation response: a review

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