miR-519 suppresses nasopharyngeal carcinoma cell proliferation by targeting oncogene URG4/URGCP

Yu, Guodong; Zhang, Tian; Jing, Ying; Bao, Qingmin; Tang, Qiang

doi:10.1016/j.lfs.2017.03.010

Cited by 28 publications

(20 citation statements)

References 16 publications

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“…Certain research groups have demonstrated that various miRNAs, including miR-212 and miR-224, promote pancreatic cancer progression via hypoxia-inducible factor 1α (27,28). By contrast, the present study revealed that miR-519 inhibited the tumorigenesis of pancreatic cancer cells, in accordance with prior conclusions (29,30). Additionally, the present study investigated and confirmed the inhibitory role of miR-519 under hypoxic conditions.…”

Section: Discussionsupporting

confidence: 87%

MicroRNA‑519 inhibits hypoxia‑induced tumorigenesis of pancreatic cancer by regulating immune checkpoint PD‑L1

et al. 2019

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Pancreatic cancer is highly prevalent and exhibits a high incidence and mortality rate. Hypoxia contributes to tumorigenesis and the progression of pancreatic cancer. To the best of our knowledge, the role of microRNA (miR)-519 has not been investigated in hypoxia-induced pancreatic cancer progression. The purpose of the present study was to elucidate the mechanism underlying miR-519-mediated regulation of pancreatic cancer progression. Reverse transcription-quantitative PCR and western blotting were performed to investigate miR-519 and programmed death ligand 1 (PD-L1) mRNA and protein levels, respectively. Additionally, a Transwell assay was performed to examine the invasiveness of PANC-1 and SW1990 cells. Cells were subsequently stained with Annexin V to determine the apoptotic rate of cells. Furthermore, bioinformatics analysis and a dual-luciferase reporter assay were performed to confirm the direct association between miR-519 and PD-L1, and a xenograft experiment was conducted to test the role of miR-519 in vivo. The results revealed that the expression levels of miR-519 in pancreatic cancer cells were reduced following hypoxia treatment. Furthermore, transfection with miR-519 mimics inhibited PANC-1 and SW1990 cell invasiveness, and induced apoptosis under hypoxic conditions. PD-L1 was also identified as a downstream target of miR-519, and rescued the miR-519 mimic-attenuated tumorigenesis of pancreatic cancer cells under hypoxic conditions. Additionally, treatment with miR-519 mimics significantly suppressed the tumor growth of PANC-1 cells. The results of the present study indicated a novel mechanism of miR-519-mediated tumorigenesis in pancreatic cancer cells under hypoxic conditions. The conclusions may be crucial for the improvement of future pancreatic cancer treatment.

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Section: Discussionsupporting

confidence: 87%

MicroRNA‑519 inhibits hypoxia‑induced tumorigenesis of pancreatic cancer by regulating immune checkpoint PD‑L1

et al. 2019

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“…The hsa_circ_0074298 downregulation promoted miR-519 expression, and miR-519 silencing restored the proliferation, migration, and GEM resistance after hsa_circ_0074298 depletion, suggesting that miR-519 had anti-tumor activity. Previous studies also found that upregulation of miR-519 inhibited cancer cell activity, including that of nasopharyngeal carcinoma and gastric cancer [21][22][23]. Together, these results strongly suggested that hsa_circ_0074298 expression promoted PC progression by sponging miR-519.…”

Section: Discussionsupporting

confidence: 53%

Knockdown of hsa_circ_0074298 suppressed the progression of pancreatic cancer by targeting the miR-519/SMOC2 axis

Chen

Wang

et al. 2020

Preprint

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BACKGROUND: Pancreatic cancer (PC) is among the most malignant tumors in the digestive system because of its fast progression, metastasis, as well as its resistance to chemotherapy. Former studies found that circRNAs that were differentially expressed were correlated with progression and gemcitabine (GEM)-resistance in PC, and hsa_circ_0074298 aberrant expression played a role in PC progression, but the regulatory mechanism was unclear. METHODS: RT-qPCR was used to detect hsa_circ_0074298 expression in PC cell lines. CCK8, colony formation, and Transwell assays were used to evaluate the effect of hsa_circ_0074298 on PC cell migration and proliferation. Bioinformatics and luciferase reporter experiments were used to characterize the regulatory mechanism. Nude mouse xenografts were generated to examine the effect of hsa_circ_0074298 on tumor growth. RESULTS: The present study showed that hsa_circ_0074298 expression increased significantly in both PC cell lines and PC tissues. Downregulation of hsa_circ_0074298 caused a significant decrease in PC cell proliferation and in nude mouse xenograft growth. Hsa_circ_0074298 silencing also increased chemotherapy sensitivity to GEM. Bioinformatics analysis indicated that hsa_circ_0074298 was a miR-519 sponge and that the SMOC2 gene was a miR-519 target. MiR-519 downregulation or SMOC2 overexpression restored cell proliferation, migration, and chemoresistance after hsa_circ_0074298 silencing. The dual luciferase reporter assay showed that hsa_circ_0074298 interacted with miR-519, and miR-519 binding to the SMOC2 3′-UTR then suppressed posttranscriptional SMOC2 expression. CONCLUSIONS: Taken together, hsa_circ_0074298 functioned as a tumor promoter through a novel miR-519/SMOC2 axis, highlighting its possibility as a potential therapy for PC.

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“…miR-519 robustly inhibits HeLa cell proliferation and induces HeLa cell senescence (27). miR-519 suppresses nasopharyngeal carcinoma cell proliferation (20). The present results demonstrated that the relative expression levels of miR-519a-3p, miR-519b-3p and miR-519c-3p were lower in primary breast cancer tissues compared with in adjacent normal tissues.…”

Section: Discussionmentioning

confidence: 52%

“…It has been reported that the miR-519 family is associated with cancer development. For example, miR-519 suppresses nasopharyngeal carcinoma cell proliferation by targeting the oncogene upregulated gene 4/upregulator of cell proliferation (20). However, the role of miR-519 in the development of breast cancer remains unknown.…”

Section: Introductionmentioning

confidence: 99%

miR‑519 regulates the proliferation of breast cancer cells via targeting human antigen�R

et al. 2019

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Breast cancer is one of the most prevalent types of cancer among women that leads to millions of deaths worldwide every year. The mechanisms of breast cancer pathogenesis remain unclear. It has been reported that aberrant expression of miR-519, is associated with breast cancer development; however, the effects of miR-519 on breast cancer cell proliferation remain unknown. Therefore, the present study aimed to determine whether miR-519 could regulate breast cancer cell proliferation. A total of 20 pairs of primary breast cancer and adjacent normal tissues were collected from patients with breast cancer. miR-519 expression level was determined by reverse transcription-quantitative polymerase chain reaction. Furthermore, miR-519 mimics or inhibitors were transfected into breast cancer MCF-7 cells in order to up-or downregulate miR-519 expression. Subsequently, human antigen R (HUR), BCL-2 and BAX protein levels were analyzed by western blotting. MCF-7 cell proliferation was assessed using MTT and colony formation assays. A luciferase assay was performed to verify whether miR-519 could directly bind to HUR mRNA. The results demonstrated that miR-519 expression level was lower in primary breast cancer tissues compared with adjacent normal tissues. Furthermore, miR-519 overexpression and downregulation inhibited and stimulated MCF-7 cell proliferation, respectively. In addition, the results from luciferase assay demonstrated that HUR was a target of miR-519. HUR overexpression could reverse the effect of miR-519 mimics on MCF-7 cell proliferation, whereas HUR silencing could rescue the effect of miR-519 inhibitors on MCF-7 cell proliferation. These findings suggested that miR-519 may regulate MCF-7 cell proliferation by targeting HUR.

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miR-519 suppresses nasopharyngeal carcinoma cell proliferation by targeting oncogene URG4/URGCP

Cited by 28 publications

References 16 publications

MicroRNA‑519 inhibits hypoxia‑induced tumorigenesis of pancreatic cancer by regulating immune checkpoint PD‑L1

MicroRNA‑519 inhibits hypoxia‑induced tumorigenesis of pancreatic cancer by regulating immune checkpoint PD‑L1

Knockdown of hsa_circ_0074298 suppressed the progression of pancreatic cancer by targeting the miR-519/SMOC2 axis

miR‑519 regulates the proliferation of breast cancer cells via targeting human antigen�R

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