MicroRNA-506 is up-regulated in the development of pancreatic ductal adenocarcinoma and is associated with attenuated disease progression

Cheng, Run Fen; Wang, Jian; Zhang, Jing Yi; Sun, Lin; Zhao, Yan; Zhi, Qiu; Sun, Bei; Sun, Yan

doi:10.1186/s40880-016-0128-9

Cited by 18 publications

(18 citation statements)

References 51 publications

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“…An increasing number of studies have reported the presence of deregulated miRNA in various human cancer types (24-26), including in glioblastoma (27,28). Furthermore, studies have demonstrated that miRNA-576-3p is an inhibitor of bladder cancer through reducing cyclin D1 (29) and may be a prognostic biomarker for breast cancer subsequent to the development of chemotherapy resistance (30).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑576‑3p inhibits the migration and proangiogenic abilities of hypoxia‑treated glioma cells through hypoxia‑inducible factor‑1α

Liu

Yan

et al. 2019

Int J Mol Med

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The most common and aggressive type of brain cancer in adults is glioblastoma multiforme (GBM), and hypoxia is a common feature of glioblastoma. As the histological features of glioma include capillary endothelial cell proliferation, they are highly prone to invading the surrounding normal brain tissue, which is often one of the reasons for the failure of treatment. However, the mechanisms involved in this process are not fully understood. MicroRNAs (miRs) are a class of non-coding RNA that are able to inhibit the malignant progression of tumor cells through the regulation of downstream genes. In the present study, the low expression of miR-576-3p was detected in glioma samples and hypoxia-treated glioma cells using a reverse transcription-quantitative polymerase chain reaction. The present study focused on the effects of miR-576-3p on hypoxia-induced glioma. The results of the functional experiments revealed that the overexpression of miR-576-3p significantly inhibited the migration and pro-angiogenic abilities of the glioma cells under hypoxic conditions (P<0.05) compared with in the lentivirus-miR-negative control group. Furthermore, luciferase reporter gene assays were used to validate the hypothesis that miR-576-3p interacts with the 3′-untranslated region of hypoxia-inducible factor-1α (HIF-1α) and induces a reduction in the protein levels of matrix metalloproteinase-2 and vascular endothelial growth factor. Rescue experiments demonstrated that the restoration of HIF-1α expression attenuated the effect of miR-576-3p on the migration and proangiogenic abilities of glioma cells. In conclusion, the present study confirms that miR-576-3p is a novel GBM inhibitor and its inhibition of the migration and proangiogenic capacity of hypoxia-induced glioma cells is mediated by HIF-1α.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‑576‑3p inhibits the migration and proangiogenic abilities of hypoxia‑treated glioma cells through hypoxia‑inducible factor‑1α

Liu

Yan

et al. 2019

Int J Mol Med

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“…It has been confirmed that miRNA quantity is a biomarker of specific diseases [18,19]. Previous studies showed that miR-506 may be involved in many activities, such as inflammation [13], cardiomyocyte dysfunction [20], malignant tumor development [21][22][23][24][25], stem cell differentiation [26], and epithelialmesenchymal transition [27], and have effects on primary biliary cirrhosis [28], rheumatoid arthritis [29], and blood vessel regeneration [30]. Therefore, miR-506 is associated with various cell biological processes, and this is consistent with the results of the present study.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-506 Is Involved in Regulation of the Occurrence of Lipopolysaccharides (LPS)-Induced Pulpitis by Sirtuin 1 (SIRT1)

Wang

Deng

et al. 2019

Med Sci Monit

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Departmental sources Background: Toothache often occurs with pulpitis. Lipopolysaccharide (LPS) is produced by gram-negative bacteria, and its accumulation is related to clinical symptoms of pain. MicroRNAs (miRNAs) display anti-inflammatory potential due to their direct regulation of cellular protein expression, which can promote inflammatory changes in dental pulp tissues. However, the mechanism of LPS-induced pulpitis is still unclear. Material/Methods: In this study, dental pulp stem cells (DPSCs) were separated and cultured from rat dental pulp tissues; then, LPS was administered to induce inflammation and activate the TLR4 pathway. Results: It was found that miR-506 was upregulated following LPS treatment in DPSCs. The inhibition of miR-506 in LPS-treated DPSCs led to attenuated inflammation and deactivation of the TLR4 pathway. Furthermore, the bioinformatic analysis and dual-luciferase reporter gene assay indicated that miR-506 could target the 3'-UTR of sirtuin 1 (SIRT1). Additionally, SIRT1 decreased in LPS-treated DPSCs, and miR-506 transfection resulted in SIRT1 upregulation. SIRT1 overexpression showed a similar inhibitory effect as that of miR-506 downregulation on inflammation and TLR4 activation in DPSCs. Conclusions: In brief, miR-506 can protect dental pulp in LPS-induced inflammation by inhibiting the SIRT1-mediated TLR4 pathway.

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“…(B) Knockdown of ZNF307 upregulated Bcl-2, and downregulated caspase-3 and Bax in the 97L-ZNFcells, compared with the controls (MoCK). in pancreatic ductal adenocarcinoma (20). Lo et al found that FoXF2 has a complex role in breast cancer and functions as either a tumor-suppressor or an oncogene depending on the breast tumor subtype (21).…”

Section: Discussionmentioning

confidence: 99%

Zinc finger protein 307 functions as a tumor-suppressor and inhibits cell proliferation by inducing apoptosis in hepatocellular carcinoma

Liang

et al. 2017

Oncology Reports

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Zinc finger protein 307 (ZNF307) is a new Krüppel-associated box zinc-finger protein gene and a member of the zinc-finger family of transcriptional factors. Notably, the role of ZNF307 and its underlying mechanisms involved in hepatocarcinogenesis are poorly investigated. In the present study, we found that the expression of ZNF307 was significantly downregulated in hepatocellular carcinoma (HCC) tissues, compared with that in adjacent non-tumor tissues. In vitro studies further demonstrated that ectopic expression of ZNF307 in HCC cell lines Bel7402 and HCCLM3 significantly reduced cell proliferation, migration and invasive ability. Concordantly, knockdown of ZNF307 increased cell proliferation, migration and invasive ability of HCC cell lines MHCC97L and QGY7701. In vivo functional studies showed that upregulation of ZNF307 expression in Bel7402 cells led to a suppression of tumorigenicity in mice, while knockdown of ZNF307 in MHCC97L cells resulted in reverse. effects. Importantly, flow cytometric analysis showed that ZNF307 overexpression increased the incidence of apoptosis, while ZNF307 knockdown decreased the incidence of apoptosis. Consistently, key regulators in apoptosis, such as caspase-3, BAX and BCL-2 were also regulated by ZNF307. Therefore, our results indicate that ZNF307 may serve as a tumor suppressor and inhibits cell proliferation of HCC via inducing apoptosis.

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MicroRNA-506 is up-regulated in the development of pancreatic ductal adenocarcinoma and is associated with attenuated disease progression

Cited by 18 publications

References 51 publications

MicroRNA‑576‑3p inhibits the migration and proangiogenic abilities of hypoxia‑treated glioma cells through hypoxia‑inducible factor‑1α

MicroRNA‑576‑3p inhibits the migration and proangiogenic abilities of hypoxia‑treated glioma cells through hypoxia‑inducible factor‑1α

MicroRNA-506 Is Involved in Regulation of the Occurrence of Lipopolysaccharides (LPS)-Induced Pulpitis by Sirtuin 1 (SIRT1)

Zinc finger protein 307 functions as a tumor-suppressor and inhibits cell proliferation by inducing apoptosis in hepatocellular carcinoma

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