MicroRNA-383 inhibits anchorage-independent growth and induces cell cycle arrest of glioma cells by targeting CCND1

Zhou, Xu; Zeng, Xingruo; Tian, Daofeng; Xu, Haitao; Cai, Qiang; Wang, Junmin; Chen, Qianxue

doi:10.1016/j.bbrc.2014.10.047

Cited by 42 publications

(41 citation statements)

References 28 publications

(27 reference statements)

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“…miR-383 targets multiple proteins and appears to function as a tumor suppressor. miR-383 has tumor suppressor effect on testicular embryonal carcinoma cell proliferation by targeting IRF1 [31] and PNUTS [32], glioma cell invasion by targeting IGF1R [33] and medulloblastoma by targeting PRDX3 [34] and CCND1 [35] and in breast cancer cell lines by targeting Gadd45g. Although further experimental evidence is required to show a direct regulation of pancreatic cancer cell proliferation, invasion and metastasis by miR38, our work sets the stage for exploring a potential miR383 tumor suppressor function in pancreatic carcinoma by its targeting of ROBO3.…”

Section: Discussionmentioning

confidence: 99%

ROBO3 promotes growth and metastasis of pancreatic carcinoma

et al. 2015

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Section: Discussionmentioning

confidence: 99%

ROBO3 promotes growth and metastasis of pancreatic carcinoma

et al. 2015

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“…Therefore, it is possible that the significant down-regulation of P53 is due to either this direct targeting of P53 or 5S rRNA involvement in modulation of MDMX-P53 signaling. It has also been indicated that miR-383 could directly target CCND1 in glioma [38]. Thus, we speculated that miR-383 might exert its role towards 5S rRNA via two different molecular mechanisms: (i).…”

Section: Discussionmentioning

confidence: 99%

Down‐regulation of 5S rRNA by miR‐150 and miR‐383 enhances c‐Myc–rpL11 interaction and inhibits proliferation of esophageal squamous carcinoma cells

et al. 2015

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a b s t r a c t 5S rRNA plays an important part in ribosome biology and is over-expression in multiple cancers. In this study, we found that 5S rRNA is a direct target of miR-150 and miR-383 in esophageal squamous cell carcinoma (ESCC). Overexpression of miR-150 and miR-383 inhibited ESCC cell proliferation in vitro and in vivo. Moreover, 5S rRNA silencing by miR-150 and miR-383 might intensify rpL11-c-Myc interaction, which attenuated role of c-Myc as an oncogenic transcriptional factor and dysregulation of multiple c-Myc target genes. Taken together, our results highlight the involvement of miRNAs in ribosomal regulation during tumorigenesis.

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“…The above results suggested that miR-383 negatively modulates IRF1 by directly binding to IRF1 3′-UTR. 28,29 However, there was more evidence suggesting that miR-383 expression was decreased in tumor tissues, including cervical cancer, 17 colon cancer, 20 prostate cancer, 21 esophageal cancer, 22 lung cancer, 30 hepatocellular cancer, 31 glioma, 32,33 invasive pituitary adenomas, 34 breast cancer, 35 pancreatic cancer, 36 serous ovarian carcinoma, and clear cell ovarian carcinoma. In lung cancer, miR-383 acted as a tumor suppressor to regulate tumor cell proliferation, invasion, and migration.…”

Section: Discussionmentioning

confidence: 99%

miR‐383 promotes cholangiocarcinoma cell proliferation, migration, and invasion through targeting IRF1

Wan

Chi

et al. 2018

J of Cellular Biochemistry

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Interferon regulatory factor 1 (IRF1) has been found to serve as a tumor suppressor in cholangiocarcinoma, and enabled prediction of clinical progression and prognosis in our previous study. The objective of the current study is to screen and identify valuable microRNAs (miR), which target IRF1 to regulate cholangiocarcinoma cell proliferation, migration, and invasion. High expression of miR-383 was observed in cholangiocarcinoma tissues and cells. Meanwhile, we found the predicted binding site of miR-383 on the IRF1 3'-untranslated region (3'-UTR) according to the miR target database. The miR-383 expression was negatively related to IRF1 messeneger RNA (mRNA) and protein expression in cholangiocarcinoma tissue samples, and miR-383 negatively regulated IRF1 mRNA and protein expression in cholangiocarcinoma cells. Subsequently, we conducted a luciferase reporter assay to prove the predicted binding site miR-383 on IRF1 3'-UTR. Moreover, the results of the rescue study suggested that IRF1 was a functional target of miR-383 involved in regulating cholangiocarcinoma cell proliferation, migration, and invasion. Finally, we evaluated the clinical and prognostic significance of miR-383 in cholangiocarcinoma cases, and found that high expression of miR-383 was correlated with advanced tumor stage, large tumor size, present vascular invasion, and metastasis, and acted as an unfavorable independent prognostic factor. In conclusion, miR-383 serves as a tumor-suppressive miR to regulate cholangiocarcinoma cell proliferation, migration, and invasion via directly targeting IRF1.

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MicroRNA-383 inhibits anchorage-independent growth and induces cell cycle arrest of glioma cells by targeting CCND1

Cited by 42 publications

References 28 publications

ROBO3 promotes growth and metastasis of pancreatic carcinoma

ROBO3 promotes growth and metastasis of pancreatic carcinoma

Down‐regulation of 5S rRNA by miR‐150 and miR‐383 enhances c‐Myc–rpL11 interaction and inhibits proliferation of esophageal squamous carcinoma cells

miR‐383 promotes cholangiocarcinoma cell proliferation, migration, and invasion through targeting IRF1

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