MicroRNA-647 promotes the therapeutic effectiveness of argon&amp;ndash;helium cryoablation and inhibits cell proliferation through targeting TRAF2 via the NF-&amp;kappa;B signaling pathway in non-small cell lung cancer

Zhang, Yunsong; Chen, Tianzi; Cai, Ying; Dong, Jianlin; Bai, Fang; Gao, Xiaojun; Tian, Li; Duan, Naiying; Liú, Dan

doi:10.2147/ott.s159337

Cited by 13 publications

(17 citation statements)

References 25 publications

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“…Moreover, we found that the cell invasion ability of glioma cells was suppressed by miR‐647 mimic. In summary, the results of the present study indicated that miR‐647 may function as a tumor suppressive role in glioma, which is consistent with its role in non‐small cell lung cancer or gastric cancer . A recent study reported that miR‐647 expression can be regulated by long non‐coding RNA PROX1‐AS1 and regulates gastric cancer progression and aggressiveness .…”

Section: Discussionsupporting

confidence: 88%

“…miR‐647 is reported to have a dual role in cancer progression in recent years. In non‐small cell lung cancer, Zhang et al . revealed that miR‐647 expression was significantly elevated in cancer tissues with argon‐helium cryoablation treatment compared to those without.…”

Section: Introductionmentioning

confidence: 99%

“…revealed that miR‐647 expression was significantly elevated in cancer tissues with argon‐helium cryoablation treatment compared to those without. In addition, miR‐647 was shown to inhibit non‐small cell lung cancer cell proliferation by arresting cell cycle via regulation of the TRAF2 and NF‐κB signaling pathway . In gastric cancer, Cao et al .…”

Section: Introductionmentioning

confidence: 99%

“…5,6 miR-647 is reported to have a dual role in cancer progression in recent years. In non-small cell lung cancer, Zhang et al 7 revealed that miR-647 expression was significantly elevated in cancer tissues with argon-helium cryoablation treatment compared to those without. In addition, miR-647 was shown to inhibit non-small cell lung cancer cell proliferation by arresting cell cycle via regulation of the TRAF2 and NF-κB signaling pathway.…”

Section: Introductionmentioning

confidence: 99%

“…In addition, miR-647 was shown to inhibit non-small cell lung cancer cell proliferation by arresting cell cycle via regulation of the TRAF2 and NF-κB signaling pathway. 7 In gastric cancer, Cao et al 8 revealed that a reduced miR-647 level was correlated with a large tumor size and worsened metastasis. Moreover, miR-647 overexpression was found to inhibit gastric cancer progression by arresting the cell cycle and inducing cell apoptosis both in vitro and in vivo.…”

Section: Introductionmentioning

confidence: 99%

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miR‐647 inhibits glioma cell proliferation, colony formation and invasion by regulating HOXA9

Qin

Tian

Chen

et al. 2020

The Journal of Gene Medicine

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Background MicroRNA‐647 (miR‐647) has been reported to regulate tumor development, although its role in glioma remains unclear. Methods miR‐647 expression in glioma cells and normal cells was measured using a quantitative real‐time polymerase chain reaction. The effects of miR‐647 expression on glioma cell proliferation, cell apoptosis, colony formation and cell invasion were measured using a cell counting kit‐8 assay, flow cytometry, a colony formation assay and a transwell invasion assay. Luciferase activity reporter and western blot assays were conducted to explore whether homeobox A9 (HOXA9) was a direct target of miR‐647. Results We found that miR‐647 expression was downregulated in glioma cell lines compared to the normal cell line. Overexpression of miR‐647 inhibits glioma cell proliferation, colony formation and cell invasion, although it promotes apoptosis in vitro. HOXA9 was validated a direct target of miR‐647 and the overexpression of HOXA9 reversed the effects of miR‐647 on glioma cell behavior. Conclusions The identification of the miR‐647/HOXA9 axis will advance our understanding underlying glioma progression and provide novel therapeutic targets for glioma treatment.

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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miR‐647 inhibits glioma cell proliferation, colony formation and invasion by regulating HOXA9

Qin

Tian

Chen

et al. 2020

The Journal of Gene Medicine

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Circular RNA circ‐CMPK1 contributes to cell proliferation of non‐small cell lung cancer by elevating cyclin D1 via sponging miR‐302e

Dong

Qian

2019

Molec Gen & Gen Med

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Background: It is well recognized that competing endogenous RNA (ceRNA) regulatory network is linked to the development and progression of cancer, including non-small cell lung cancer (NSCLC). Herein, we aimed to explore the functional role of circ-CMPK1/miR-302e/cyclin D1 ceRNA signaling in NSCLC. Methods: GEO database (GSE10 2287) was utilized to screen differentially expressed miRNAs in NSCLC. Quantitative reverse transcription PCR (qRT-PCR) and western blotting assays were used to determine gene expression. Cell proliferation analysis was performed with Cell Counting Kit-8 (CCK-8) and cell cycle assays.Luciferase reporter and RNA pull-down assays were conducted to identify the interaction among circ-CMPK1, miR-302e, and cyclin D1. Xenograft tumor model was established to evaluate the role of circ-CMPK1/miR-302e/cyclin D1 axis in vivo. Results: miR-302e expression was significantly down-regulated in NSCLC cell lines and tissues and its decrease was closely associated with aggressive clinicopathological features and unfavorable outcome. Overexpression and knockdown of miR-302e obviously retarded and enhanced the growth of NSCLC, respectively. Furthermore, we found that miR-302 was sponged by circular RNA CMPK1 (circ-CMPK1, hsa_ circ_0012384), which was remarkably up-regulated in NSCLC and predicted poor prognosis. Circ-CMPK1 was capable to promote NSCLC cells proliferation by increasing the expression of cyclin D1 via inhibiting miR-302 activity. Moreover the miR-302e-mediated tumor inhibition could be effectively counteracted by ectopic expression of circ-CMPK1 or cyclin D1 both in vitro and in vivo. Conclusion: Our data demonstrate for the first time that circ-CMPK1/miR-302e/cyclin D1 signaling plays an essential regulatory role in NSCLC and targeting this axis may be an efficacious avenue for treatment of NSCLC patients. K E Y W O R D Sbiomarker, ceRNA, circular RNA, microRNA, NSCLC, proliferation 2 of 10 | CUI et al.

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RETRACTED: TRAF2 gene silencing induces proliferation and represses apoptosis of nucleus pulposus cells in rats with intervertebral disc degeneration

Zhou

Chen³

et al. 2021

Life Sciences

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MicroRNA-647 promotes the therapeutic effectiveness of argon–helium cryoablation and inhibits cell proliferation through targeting TRAF2 via the NF-κB signaling pathway in non-small cell lung cancer

Cited by 13 publications

References 25 publications

miR‐647 inhibits glioma cell proliferation, colony formation and invasion by regulating HOXA9

miR‐647 inhibits glioma cell proliferation, colony formation and invasion by regulating HOXA9

Circular RNA circ‐CMPK1 contributes to cell proliferation of non‐small cell lung cancer by elevating cyclin D1 via sponging miR‐302e

RETRACTED: TRAF2 gene silencing induces proliferation and represses apoptosis of nucleus pulposus cells in rats with intervertebral disc degeneration

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