MiR-376c-3p regulates the proliferation, invasion, migration, cell cycle and apoptosis of human oral squamous cancer cells by suppressing HOXB7

Wang, Kai; Jin, Jun; Ma, Tengxiao; Zhai, Hong-feng

doi:10.1016/j.biopha.2017.04.050

Cited by 34 publications

(33 citation statements)

References 34 publications

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“…For instance, miR-122-5p serves as a tumor suppressor and negatively regulates cancer cell migration (28,29). Previous studies also demonstrated that miR-210-3p, miR-296-5p, and miR-376c-3p inhibited cancer cell migration (30)(31)(32). Our study showed that MEXs displayed significantly greater migration tendencies than UEXs.…”

Section: Discussionsupporting

confidence: 66%

Maternal and umbilical cord serum‐derived exosomes enhance endothelial cell proliferation and migration

et al. 2018

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We investigated the role of exosomes derived from maternal and umbilical cord blood in the regulation of angiogenesis. We report here that both maternal exosomes (MEs) and umbilical exosomes (UEs) significantly enhance HUVEC proliferation, migration, and tube formation. Importantly, ME-treated HUVECs (MEXs) displayed significantly increased migration, but not proliferation or tube formation, compared with UE-treated HUVECs (UEXs). We found that the expression of a subset of migration-related microRNAs (miRNAs), including miR-210-3p, miR-376c-3p, miR-151a-5p, miR-296-5p, miR-122-5p, and miR-550a-5p, among others, were significantly increased or decreased in UEs, and this altered expression was likely correlated with the differential regulation of HUVEC migration. We also found that the mRNA expression of hepatocyte growth factor (HGF) was up-regulated in MEXs and UEXs and, moreover, that inhibiting HGF partially abolished the enhanced cell migration induced by UEs. Our results suggest that both MEs and UEs greatly enhanced endothelial cell (EC) functions and differentially regulated EC migration, which was mostly attributed to the different expression profiles of exosomal miRNA. These findings highlight the importance of exosomes in the regulation of angiogenesis during pregnancy. Exosomal miRNAs, in particular, may be of great significance for the regulation of angiogenesis in maintaining normal pregnancy.-Jia, L., Zhou, X., Huang, X., Xu, X., Jia, Y., Wu, Y., Yao, J., Wu, Y., Wang, K. Maternal and umbilical cord serum-derived exosomes enhance endothelial cell proliferation and migration.

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Section: Discussionsupporting

confidence: 66%

Maternal and umbilical cord serum‐derived exosomes enhance endothelial cell proliferation and migration

et al. 2018

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“…Moreover, the expression of miR-376c-3p was reduced in International Neuroblastoma Staging System (INSS) stage 4 compared to stage 1-2 in a cohort of 226 primary neuroblastoma tumors (32). However, Earlier reports from various cancers have demonstrated the dual nature of miR-376c-3p to act as either the oncogenic or the tumor suppressive miRNA depending on the cellular contexts (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20). miR-376c-3p is downregulated in multiple human cancers, including prostate cancer (11), cervical cancer (10), oral squamous cell carcinoma (12), intrahepatic cholangiocarcinoma (13), melanoma (14), osteosarcoma (15) and gliomas (16).…”

Section: Discussionmentioning

confidence: 99%

“…In these cancers, miR-376-3p has been shown to target a set of genes including B-cell-specific moloney murine leukemia virus insertion site 1 (BMI1), homeobox B7 (HOXB7), growth factor receptor-bound protein 2 (GRB2), transforming growth factor-alpha (TGFA), liver receptor homolog-1 (LRH-1), insulin growth factor 1 receptor (IGF1R) and activin receptor-like kinase 7 (ALK7). Other than affecting cell growth and proliferation, these genes act as important mediators of cell invasion (10,12,15,20), migration (11)(12)(13)(14), cell cycle arrest (10), apoptosis (12) and chemoresistance (19).…”

Section: Discussionmentioning

confidence: 99%

“…They are expressed in placenta, developing embryos, and adult tissues (8). The expression of miR-376c is downregulated in many human malignancies including cervical cancer (10), prostate cancer (11), oral squamous cell carcinoma (12), intrahepatic cholangiocarcinoma (13), melanoma (14), osteosarcoma (15) and gliomas (16). However, it has been shown that miR-376c is upregulated and it act as oncogenic in acute myeloid leukemia (17) and gastric cancer (18).…”

Section: Introductionmentioning

confidence: 99%

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Hsa‑miR‑376c‑3p targets Cyclin D1 and induces G1‑cell cycle arrest in neuroblastoma cells

et al. 2018

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High-risk neuroblastoma is the most aggressive form of cancer in children. The estimated survival of children with high-risk neuroblastoma is 40-50% compared with low and intermediate risk neuroblastoma, which is >98 and 90-95%, respectively. In addition, patients with high-risk neuroblastoma often experience relapse following intensive treatments with standard chemotherapeutic drugs. Therefore alternative strategies are required to address this problem. MicroRNAs (miRNAs/miRs) are small, endogenously expressed non-coding RNAs, which when deregulated have been demonstrated to serve significant roles in the tumorigenesis of a number of different types of cancer. Results from a previous deep sequencing study identified 22 downregulated miRNAs from the 14q32 miRNA cluster differentially expressed in neuroblastoma cell lines isolated from 6 patients at diagnosis and at relapse following intensive treatments. miR-376c-3p is one of the 22 miRNAs that was downregulated in the majority of the cell lines isolated from patients post treatment. The present study employed reverse transcription-quantitative polymerase chain reaction (RT-qPCR) to quantify the basic expression of miR-376c-3p in 6 neuroblastoma cell lines. The functional role of miR-376c-3p in the neuroblastoma cell lines was evaluated by alamar blue-cell viability and propidium iodide-flow cytometric assays. In addition, luciferase reporter assays, RT-qPCR and western blotting were performed to identify and quantify the targets of miR-376c-3p in neuroblastoma cell lines. Ectopic expression of miR-376c-3p led to significant inhibition of cell viability and G1-cell cycle arrest in multiple neuroblastoma cell lines by reducing the expression of cyclin D1, an oncogene critical for neuroblastoma pathogenesis. The results of the present study provide novel insights into the functional role of miR-376c-3p and suggest new approaches for the treatment of neuroblastoma.

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“…Mechanically, we speculated that circPIP5K1A might post-transcriptionally modulate gene expression by functioning as a ceRNA in GC based on the data that circPIP5K1A was mainly distributed in cytoplasm, and thereby it was primarily needed to find out the specific miRNA. Subsequently, through bioinformatics prediction and molecular experiments, miR-376c-3p was screened out due to its notable high binding ability with circPIP5K1A and its close association with the progression of human malignancies [25][26][27]. Then miR-376c-3p was confirmed to be dramatically downregulated in GC cells.…”

Section: Discussionmentioning

confidence: 99%

CircPIP5K1A facilitates gastric cancer progression via miR-376c-3p/ZNF146 axis

Cong

Zhang

et al. 2020

Cancer Cell Int

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Background: Recently, many emerging circular RNAs (circRNAs) have been studied in human malignancies, including gastric cancer (GC). Researches concerning cancers have revealed that aberrant expression of circRNAs play a big part in tumorigenesis and development of diverse malignant tumors. Although hsa_circ_0014130 (circPIP5K1A) has been confirmed to be closely related to non-small cell lung cancer (NSCLC) progression, the knowledge of its function on GC progression remains unclear. Therefore, it is of great interest to uncover the underlying role of circPIP5K1A in GC. Methods: The expression and characteristic of circPIP5K1A were separately analyzed by RT-qPCR, nucleic acid electrophoresis, RNase R and Actinomycin D treatment. CCK-8, colony formation, EdU, transwell, TUNEL, flow cytometry, luciferase reporter, RIP and RNA pull-down assays were employed to testify the regulatory role of circPIP5K1A in GC. Results: In current study, circPIP5K1A, featured with closed-loop structure, was proved to be highly expressed in tissues and cells of GC. Loss-of-function assays depicted that silencing circPIP5K1A suppressed GC development. Followup mechanism tests unveiled that circPIP5K1A bound with miR-376c-3p and inhibition of miR-376c-3p reversed circ-PIP5K1A downregulation-mediated effect on GC progression. Additionally, ZNF146 was verified to be the downstream molecule of circPIP5K1A/miR-376c-3p axis in modulating GC progression. Conclusions: circPIP5K1A stimulates GC progression by sponging miR-376c-3p to upregulate ZNF146 expression.

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MiR-376c-3p regulates the proliferation, invasion, migration, cell cycle and apoptosis of human oral squamous cancer cells by suppressing HOXB7

Cited by 34 publications

References 34 publications

Maternal and umbilical cord serum‐derived exosomes enhance endothelial cell proliferation and migration

Maternal and umbilical cord serum‐derived exosomes enhance endothelial cell proliferation and migration

Hsa‑miR‑376c‑3p targets Cyclin D1 and induces G1‑cell cycle arrest in neuroblastoma cells

CircPIP5K1A facilitates gastric cancer progression via miR-376c-3p/ZNF146 axis

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