MicroRNA-384 is lowly expressed in human prostate cancer cells and has anti-tumor functions by acting on HOXB7

Hong, Zhiming; Fu, Wei; Wang, Quan; Zeng, Yangling; Li-jing, QI

doi:10.1016/j.biopha.2019.108822

Cited by 13 publications

(12 citation statements)

References 24 publications

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“…24,25 miR-384 is a tumor suppressor, which is down-regulated in osteosarcoma and papillary thyroid cancer, and inhibits tumor growth. 26,27 In PCa, miR-384 expression is reported to be down-regulated, and it suppresses tumor growth in vivo and in vitro, 28 which is consistent with the demonstrations in the present research. Reportedly, lncRNAs can act as an endogenous 'sponge' to regulate miRNA activity and play a regulatory role in tumor progression.…”

Section: Discussionsupporting

confidence: 91%

“…In pancreatic cancer, HOXB7 facilitates the invasion of cancer cells by inducing the phosphorylation of ERK1/2 38 . In PCa, HOXB7 expression is up‐regulated, and its overexpression is closely related to the short survival time of patients; furthermore, HOXB7 can promote the proliferation and migration of PCa cells, and is negatively regulated by miR‐384 28 . In the present study, we confirmed again that miR‐384 could targetedly regulate HOXB7, and further investigations revealed that knocking down SNHG8 could repress HOXB7 expression, while miR‐384 inhibitors could reverse this effect.…”

Section: Discussionmentioning

confidence: 99%

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Long non‐coding RNA SNHG8 promotes prostate cancer progression through repressing miR‐384 and up‐regulating HOXB7

Shi

Zhang

Song

et al. 2021

The Journal of Gene Medicine

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Background Multiple long non‐coding RNAs (lncRNAs) have been demonstrated to function as vital regulators in the progression of prostate cancer (PCa). In the present study, we aimed to probe the function of lncRNA small nucleolar RNA host gene 8 (SNHG8) in PCa progression. Methods A quantitative real‐time polymerase chain reaction and western blotting were utilized to measure SNHG8, microRNA‐384 (miR‐384) and homeobox B7 (HOXB7) expression. Call‐couting kit‐8 and bromodeoxyuridine experiments were employed to evaluate PCa cell proliferation. Transwell experiments were performed to detect PCa cell migration and invasion. Dual‐luciferase reporter experiments and RNA immunoprecipitation experiments were conducted to determine the targeting relationships among miR‐384, SNHG8 and HOXB7. Results SNHG8 was up‐regulated in PCa tissues and cells. Silencing of SNHG8 suppressed the proliferation, migration and invasion of PCa cells. SNHG8 functioned as a molecular sponge to repress miR‐384. The effects of SNHG8 knockdown on PCa cell proliferation, migration and invasion were counteracted by miR‐384 inhibition. HOXB7 was confirmed to be a target gene of miR‐384. SNHG8 knockdown repressed HOXB7 expression via targeting miR‐384. Conclusions SNHG8 promotes PCa cell proliferation, migration and invasion via decoying miR‐384 and up‐regulating HOXB7.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA SNHG8 promotes prostate cancer progression through repressing miR‐384 and up‐regulating HOXB7

Shi

Zhang

Song

et al. 2021

The Journal of Gene Medicine

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“…In this study, we adopted qRT-PCR technology in cell experiments to find that, compared with normal human gastric cells, miR-134-5p and miR-384 were both downregulated in GC cell lines. Studies have revealed that miR-384 decreased significantly in laryngeal carcinoma, breast cancer and GC cells, [19][20][21] and Lai et al confirmed that overexpression of miR-384 inhibited hepatocellular carcinoma progression. 22 Subsequently, we silenced and overexpressed miR-134-5p and miR-384 in KATO III to find that miR-384 or miR-134-5p overexpression could inhibit cell proliferation and invasion, promote apoptosis, and inhibit cell EMT-related molecular markers.…”

Section: Discussionmentioning

confidence: 93%

<p>Effects of miR-384 and miR-134-5p Acting on YY1 Signaling Transduction on Biological Function of Gastric Cancer Cells</p>

Zhong

Wang

et al. 2020

OTT

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Objective: To explore the related influencing mechanism of miR-384 and miR-134-5p acting on Yin Yang 1 (YY1) signaling transduction on the biological function of gastric cancer (GC) cells. Methods: miR-384, miR-134-5p and YY1 levels in human GC cell lines KATO III, MKN-45, SNU-1 and normal gastric cell line GES-1 were measured by polymerase chain reaction (PCR). Dual luciferase reporter (DLR) gene assay and Western blot (WB) were employed for correlation analysis between miR-384, miR-134-5p and YY1. miR-384-inhibitor, miR-384mimics, empty plasmid (miRNA-NC) and sh-YY1 were transfected into KATO III cells. Cell proliferation was determined by 3-(4,5-Dimethylthiazolyl-2)-2,5-Diphenyl Tetrazolium Bromide (MTT), cell invasion was measured by Transwell, and apoptosis was analyzed by flow cytometry (FC). Results: In KATO III, MKN-45 and SNU-1 cell lines, YY1 was upregulated while miR-384 and miR-134-5p were downregulated (P<0.001). The expression of miR-134-5p in the miR-134-5p-inhibitor group was significantly lower (P<0.001), while that in the miR-134-5pmimics group was significantly higher (P<0.001). The expression of miR-384 in the miR-384-inhibitor group was significantly lower (P<0.001), and that in the miR-384-mimics group was significantly higher as compared to the NC group (P<0.001). Both miR-384 and miR-134-5p overexpression could inhibit cell proliferation and invasion, and promote apoptosis. As detected by WB, overexpressed miR-384 and miR-134-5p inhibited the expression of EMT-related molecular markers. Compared with sh-YY1, the number of cells in S phase decreased, the pro-apoptotic proteins boosted statistically, and the anti-apoptotic proteins declined notably after transfecting miR-134-5p-mimics/sh-YY1 or miR-384-mimics/sh-YY1 (P<0.05). The tumor growth rate of nude mice in miR-134-5p/sh-YY1 and miR-384/sh-YY1 groups were significantly lower than those in sh-YY1 group (all P<0.001). Conclusion: By targeting YY1 signaling transduction, miR-134-5p and miR-384 can alter the growth and apoptosis of GC cells, which are promising targets for new therapeutics of GC.

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“…6 Interestingly, it has been reported to inhibit HOBX7 mRNA stability in human prostate cancer cells. 7 However, its role in many other cancers, such as OS, remains in the dark.…”

Section: Introductionmentioning

confidence: 99%

MiR-384 Inhibits Malignant Biological Behavior Such as Proliferation and Invasion of Osteosarcoma by Regulating IGFBP3

Tan

Chen

et al. 2020

Technol Cancer Res Treat

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Osteosarcoma is the most common primary malignant bone tumor in the clinic. It is more common in children and adolescents. It has high malignancy, early metastasis rate, rapid disease progression, and high mortality. Although past years have witnessed the great improvement in the treatments of osteosarcoma, there remains a long way to go. MicroRNAs affect the malignant biological behaviors such as tumor proliferation and metastasis by regulating their target genes. In this study, we investigated the role and mechanism of miR-384 in osteosarcoma. Quantitative real-time polymerase chain reaction assay was performed to detect the expression of miR-384 and insulin-like growth factor binding protein 3 in osteosarcoma tissues and cell lines and established its correlation with osteosarcoma tumor progression and metastasis. To probe whether miR-384 played a tumor suppression role in osteosarcoma, we carried out gain-of-function and loss-of-function assays. Cell Counting Kit-8, cell colony formation, and transwell assays were carried out to determine the cells proliferation and invasion, respectively. Western blot was used to detect the changes of epithelial–mesenchymal transition marker proteins and insulin-like growth factor binding protein 3. MiR-384 was downregulated in osteosarcoma tissues and cell lines. MiR-384 was overexpressed in G292 cells transfected with miR-384 mimics and knocked down in Saos-2 cells with small hairpin RNA targeting miR-384. Ectopic expression of miR-384 inhibited osteosarcoma cell proliferation, colony formation, and invasion. E-cadherin was brought to a decrease whereas N-cadherin and Snail to an increase under the silent expression of miR-384, while overexpression of miR-384 led to an opposite result. MiR-384 could regulate insulin-like growth factor binding protein 3 expression in osteosarcoma. Quantitative polymerase chain reaction and Western blotting results validated that miR-384 knockdown downgrades both messenger RNA and protein levels of insulin-like growth factor binding protein 3 in G292 cells, while miR-384 upregulation exerted an opposite effect in Saos-2 cells. Insulin-like growth factor binding protein 3 was upregulated in osteosarcoma tissues and osteosarcoma cell lines compared with normal ones. Through the bioinformatics database found that the upstream transcriptional regulator of insulin-like growth factor binding protein 3 is MECP2. So miR-384 can directly inhibit MECP2 and then promote the expression of insulin-like growth factor binding protein 3. These results suggested that miR-384 might be a potential therapeutic targets and biomarker in osteosarcoma.

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MicroRNA-384 is lowly expressed in human prostate cancer cells and has anti-tumor functions by acting on HOXB7

Cited by 13 publications

References 24 publications

Long non‐coding RNA SNHG8 promotes prostate cancer progression through repressing miR‐384 and up‐regulating HOXB7

Long non‐coding RNA SNHG8 promotes prostate cancer progression through repressing miR‐384 and up‐regulating HOXB7

<p>Effects of miR-384 and miR-134-5p Acting on YY1 Signaling Transduction on Biological Function of Gastric Cancer Cells</p>

MiR-384 Inhibits Malignant Biological Behavior Such as Proliferation and Invasion of Osteosarcoma by Regulating IGFBP3

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