MicroRNA-92b represses invasion-metastasis cascade of esophageal squamous cell carcinoma

Ma, Gang; Jing, Chao; Lin, Li; Huang, Furong; Ding, Fang; Wang, Baona; Lin, Dongmei; Luo, Aiping; Liu, Zhihua

doi:10.18632/oncotarget.7747

Cited by 48 publications

(51 citation statements)

References 43 publications

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“…Among these miRs, it has been observed that miR-92b serves a role in certain types of human cancer (17,18). miR-92b promotes the proliferation, migration and invasion of glioma cells, and induces apoptosis via regulation of the phosphatase and tensin homolog (PTEN)/protein kinase B signaling pathway (17).…”

Section: Introductionmentioning

confidence: 99%

“…miR-92b promotes the proliferation, migration and invasion of glioma cells, and induces apoptosis via regulation of the phosphatase and tensin homolog (PTEN)/protein kinase B signaling pathway (17). Additionally, miR-92b represses the invasion and metastasis of esophageal squamous cell carcinoma (ESCC) in vitro and in vivo , and higher expression of miR-92b in ESCC tissue is inversely correlated with lymph node metastasis and indicates better patient prognosis (18). Recently, it has been demonstrated that miR-92b promotes the malignant phenotype of osteosarcoma cells by inhibiting the expression of reversion-inducing, cysteine-rich protein with kazal motifs (RECK) (19).…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA‑92b promotes cell proliferation and invasion in osteosarcoma by directly targeting Dickkopf‑related protein 3

Zhou

Feng

et al. 2017

Exp Ther Med

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Deregulation of microRNA-92b (miR-92b) has been implicated in osteosarcoma. However, the underlying regulatory mechanism of miR-92b in osteosarcoma growth and metastasis remains largely unclear. In the present study, reverse transcription-quantitative polymerase chain reaction and western blotting were used to measure mRNA and protein expression. MTT and Transwell assays were conducted to determine cell proliferation and invasion, and a luciferase reporter assay was performed to confirm the association between miR-92b and Dickkopf3-related protein (DKK3). The results demonstrated that miR-92b was significantly upregulated in osteosarcoma tissues compared with matched adjacent non-tumor tissues. Additionally, high miR-92b levels were significantly associated with lung metastasis and advanced tumor, node, metastasis stage (P<0.05) but not with age, sex, tumor size, location, serum lactate dehydrogenase or serum alkaline phosphatase. miR-92b expression was also significantly upregulated in osteosarcoma cell lines compared with normal osteoblast cells. Knockdown of miR-92b significantly inhibited the proliferation and invasion of osteosarcoma U2OS cells (P<0.01). By contrast, overexpression of miR-92b significantly increased U2OS cell proliferation and invasion (P<0.01). DKK3 was identified as a target gene of miR-92b and it was demonstrated that DKK3 expression was negatively regulated by miR-92b in U2OS cells. Restoration of DKK3 expression abrogated the increased proliferation and invasion of U2OS cells induced by miR-92b overexpression. Notably, DKK3 was significantly downregulated in osteosarcoma tissues compared with adjacent non-tumor tissues and its expression was inversely correlated to miR-92b levels in osteosarcoma tissues. Taken together, these data indicate that miR-92b promotes cell proliferation and invasion in osteosarcoma by targeting DKK3. Therefore, miR-92b may become a potential therapeutic target for osteosarcoma.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNA‑92b promotes cell proliferation and invasion in osteosarcoma by directly targeting Dickkopf‑related protein 3

Zhou

Feng

et al. 2017

Exp Ther Med

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“…Protein extraction and Western blotting were conducted as previously reported . The following antibodies were used in the present study: JNK (Catalog: A11119; ABclonal Technology); p‐JNK (Catalog: AP0808; ABclonal Technology); MEK5 (Catalog: A6953; ABclonal Technology); p‐ERK1/2 (Catalog: AP0472; ABclonal Technology); ERK1/2 (Catalog: D160317; Sangon Biotech); p‐38 (Catalog: D155224; Sangon Biotech); p‐p38 (Catalog: D155179; Sangon Biotech); ERK5 (Catalog: D120601; Sangon Biotech); β‐Actin (Catalog: AC026; ABclonal Technology).…”

Section: Methodsmentioning

confidence: 99%

“…The in-vitro invasion assay was performed in 24-well Boyden chambers (Corning Inc) pre-coated with the presence of Matrigel (BD Biosciences), as previously described. 33 Cells were counted from at least four randomly selected microscopic fields.…”

Section: Cell Invasion Assaymentioning

confidence: 99%

Melittin inhibits proliferation, migration and invasion of bladder cancer cells by regulating key genes based on bioinformatics and experimental assays

Yao

Zhang

et al. 2019

J Cellular Molecular Medi

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The antitumour effect of melittin (MEL) has recently attracted considerable attention. Nonetheless, information regarding the functional role of MEL in bladder cancer (BC) is currently limited. Herein, we investigated the effect of MEL on critical module genes identified in BC. In total, 2015 and 4679 differentially expressed genes (DEGs) associated with BC were identified from the GSE31189 set and The Cancer Genome Atlas database, respectively. GSE‐identified DEGs were mapped and analysed using Gene Ontology and Kyoto Encyclopaedia of Genes and Genomes analyses to determine BC‐involved crucial genes and signal pathways. Coupled with protein–protein interaction network and Molecular Complex Detection analyses, Modules 2 and 4 were highlighted in the progression of BC. In in‐vitro experiments, MEL inhibited the proliferation, migration, and invasion of UM‐UC‐3 and 5637 cells. The expression of NRAS, PAK2, EGFR and PAK1 in Module 4—enriched in the MAPK signalling pathway—was significantly reduced after treatment with MEL at concentrations of 4 or 6 μg/mL. Finally, quantitative reverse transcription‐polymerase chain reaction and Western blotting analyses revealed MEL inhibited the expression of genes at the mRNA (ERK1/2, ERK5, JNK and MEK5), protein (ERK5, MEK5, JNK and ERK1/2) and phosphorylation (p‐ERK1/2, p‐JNK, and p‐38) levels. This novel evidence indicates MEL exerts effects on the ERK5‐MAK pathway—a branch of MAPK signalling pathway. Collectively, these findings provide a theoretical basis for MEL application in BC treatment.

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“…The involvement of miR-92b in tumor cell biology has been reported in many tumors including brain primary tumors, 25 neuroblastoma, 26 glioblastoma, 27 non-small cell lung cancer, 28 oral squamous cell carcinoma, 29 esophageal squamous cell carcinoma, 30 bladder cancer, 31 and colorectal carcinoma. 32 A previous study F I G U R E 4 Impact of hepatoma-derived exosomes and exosomal miR-92b on NK cell activity.…”

Section: Discussionmentioning

confidence: 99%

Circulating exosomal miR-92b: Its role for cancer immunoediting and clinical value for prediction of posttransplant hepatocellular carcinoma recurrence

Nakano

Chen

Wang

et al. 2019

American Journal of Transplantation

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A recurrence of hepatocellular carcinoma (HCC) after living donor liver transplantation (LDLT) is one of the major concerns reflecting the higher mortality of HCC. This study aimed to explore the impact of circulating exosomes on HCC development and recurrence. One-shot transfusion of hepatoma serum to naïve rats induced liver cancer development with gradual elevation of alpha-fetoprotein (AFP), but exosome-free hepatoma serum failed to induce AFP elevation. The microarray analysis revealed miR-92b as one of the highly expressing microribonucleic acids in hepatoma serum exosomes. Overexpression of miR-92b enhanced the migration ability of liver cancer cell lines with active release of exosomal miR-92b. The hepatoma-derived exosomal miR-92b transferred to natural killer (NK) cells, resulting in the downregulation of CD69 and NK cell-mediated cytotoxicity. Furthermore, higher expression of miR-92b in serum exosomes was confirmed in HCC patients before LDLT, and its value at 1 month after LDLT was maintained at a higher level in the patients with posttransplant HCC recurrence. In summary, we demonstrated the impact of circulating exosomes on liver cancer development, partly through the suppression of CD69 on NK cells by hepatoma-derived exosomal miR-92b. The value of circulating exosomal miR-92b may predict the risk of posttransplant HCC recurrence. K E Y W O R D Sbasic (laboratory) research/science, biomarker, cancer/malignancy/neoplasia: risk factors, cellular biology, immunobiology, liver transplantation/hepatology, microarray/gene array, molecular biology: micro RNA, natural killer (NK) cells/NK receptors, translational research/ science 1 | INTRODUC TI ON Hepatocellular carcinoma (HCC) is the second leading cause of death from cancer in the world. 1 In general, malignant tumor regions are treated by radiofrequency ablation (RFA) or transarterial embolization (TAE) and/or removed by surgical resection.Our group compared the disease-free survival of HCC patients between surgical resection and RFA in the Barcelona Clinic Liver

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MicroRNA-92b represses invasion-metastasis cascade of esophageal squamous cell carcinoma

Cited by 48 publications

References 43 publications

MicroRNA‑92b promotes cell proliferation and invasion in osteosarcoma by directly targeting Dickkopf‑related protein 3

MicroRNA‑92b promotes cell proliferation and invasion in osteosarcoma by directly targeting Dickkopf‑related protein 3

Melittin inhibits proliferation, migration and invasion of bladder cancer cells by regulating key genes based on bioinformatics and experimental assays

Circulating exosomal miR-92b: Its role for cancer immunoediting and clinical value for prediction of posttransplant hepatocellular carcinoma recurrence

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