Circular RNA_0076977 contributes to oral squamous cell carcinoma progression through mediating microRNA-802 axis.

OBJECTIVE: The study aims to explore the role and the mechanism of circ_0076977 regulating oral squamous cell carcinoma progression (OSCC) progression. DESIGN: Reverse transcription-quantitative polymerase chain reaction and western blot assays were conducted to analyze RNA and protein expression. Cell proliferation was analyzed by 5-ethynyl-2'-deoxyuridine incorporation and colony formation assays. Cell apoptosis was measured by flow cytometry. Tube formation assay was conducted to analyze cell angiogenesis ability. Transwell assays were performed to detect cell migration and invasion abilities. Dual-luciferase reporter assay was implemented to verify the target relationship. RESULTS: Circular (circ)_0076977 was abnormally up-regulated in OSCC tissues and cell lines. Circ_0076977 absence inhibited the proliferation, angiogenesis, migration, and invasion and induced the apoptosis of oral squamous cell carcinoma (OSCC) cells. Circ_0076977 knockdown blocked xenograft tumor growth. miR-802 was a direct target of circ_0076977, and circ_0076977 knockdown restrained OSCC progression largely by up-regulating miR-802. miR-802 directly interacted with myosin VI (MYO6) mRNA, and MYO6 was negatively modulated by miR-802 in OSCC cells. miR-802 overexpression reduced the malignant potential of OSCC cells largely by down-regulating MYO6. Circ_0076977 could up-regulate MYO6 expression by absorbing miR-802 in OSCC cells. CONCLUSION: Circ_0076977 was up-regulated in OSCC tissues and cell lines, and high circ_0076977 expression contributed to OSCC progression by targeting miR-802/MYO6 axis.

[Retracted] miR­802 inhibits the aggressive behaviors of non­small cell lung cancer cells by directly targeting FGFR1.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the data panels showing results from flow cytometric experiments in Figs. 2D, 4D and 5D, and tumor images shown in Fig. 7A, were strikingly similar to data that had appeared in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to International Journal of Oncology, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Oncology54: 2211­2221, 2019; DOI: 10.3892/ijo.2019.4765].

Long noncoding RNA TRG-AS1 protects against glucocorticoid-induced osteoporosis in a rat model by regulating miR-802-mediated CAB39/AMPK/SIRT-1/NF-κB axis.

The long-term treatment of glucocorticoids is a common cause of osteoporosis (OP). This study concentrated on inquiring into the regulatory role and potential mechanisms of TRG-AS1 on dexamethasone (Dex)-induced OP in rats. We adopted Dex to treat rat osteoblasts and rats to simulate in-vitro and in-vivo OP models, respectively. Gain-of-function assays of TRG-AS1, miR-802 and CAB39 were constructed in rat osteoblasts to make certain the influence of TRG-AS1, miR-802 and CAB39 on differentiation, proliferation and apoptosis of rat osteoblasts. TRG-AS1 and CAB39 were down-regulated in the Dex-induced OP model in rats, in contrast to miR-802. Overexpression of TRG-AS1 restrained Dex-induced inhibition of osteogenic differentiation, promoted CAB39/AMPK/SIRT-1 and inhibited NF-κB, while overexpression of miR-802 bridled the inhibitory effect of TRG-AS1 on OP. miR-802 was targeted by TRG-AS1, and inhibited CAB39. Inhibition of either AMPK or SIRT-1 abated the osteogenic differentiation-promoting effect of CAB39. Animal experiments displayed that overexpressing TRG-AS1 alleviated Dex-induced OP in rats. In conclusion, up-regulation of TRG-AS1 protected against glucocorticoid-induced OP in rats by modulating the miR-802-mediated CAB39/AMPK/SIRT-1/NF-κB axis.

Bioinformatic Investigation of Micro RNA-802 Target Genes, Protein Networks, and Its Potential Prognostic Value in Breast Cancer.

Background: An increasing number of studies have suggested that unveiling the molecular network of miRNAs may provide novel therapeutic targets or biomarkers. In this study, we investigated the probable molecular functions that are related to microRNA-802 (miR-802) and evaluated its prognostic value in breast cancer utilizing bioinformatics tools. Methods: PPI network, pathway enrichment and transcription factor analysis were applied to obtain hub genes among overlapping genes of four miRNA target prediction databases. Prognosis value assessments and expression analysis of hub genes using bioinformatics tools, as well as their literature validation were performed. Results: Our results showed a significant correlation of the miR-802 overexpression with poor patient survival rate (BC, p=2.7e-5). We determined 247 target genes significant for GO and KEGG terms. Analysis of TFs by TRUST showed that RUNX3, FOXO3, and E2F1 are possible TFs that regulate the miR-802 expression and target genes network. According to our analysis; 21 genes might have an important function in miR-802 molecular processes and regulatory networks. The result shows that among these 21 genes, 8 genes (CASC3, ITGA4, AGO3, TARDBP, MED13L, SF1, SNRPE and CRNKL1) are positively correlated with patient survival. Therefore these genes could be considered and experimentally evaluated as a prognostic biomarker for breast cancer. Conclusion: The comprehensive bioinformatics study on miR-802 target genes provided insight into miR-802 mediated pathways and processes. Furthermore, representing candidate target genes by prognostic values indicates the potential clinical application of miR-802 in breast cancer.

MicroRNA-802 promotes the progression of osteosarcoma through targeting p27 and activating PI3K/AKT pathway

PurposeIncreasing evidences suggest dysfunctions of microRNAs (miRNAs) are playing important part in tumors. Therefore, the role of miR-802 in osteosarcoma (OS) was exploited. The object was to evaluate the effect of miR-802 and verify its influence on p27 Kip1 (p27) in OS.MethodsRT-qPCR experiment was used to detect miR-802 and p27 expression in OS tissues and cells. We explored the function of miR-802 through Transwell assays. The phosphoinositide 3-kinase (PI3K)/AKT serine/threonine kinase pathway and epithelial–mesenchymal transition (EMT) was detected by Western blot assays. Luciferase assay was used to testify the target of miR-802.ResultsMiR-802 expression was elevated in OS, which was related to poor clinical outcome in OS patients. MiR-802 overexpression promoted OS migration, invasion and EMT. Further, p27 is a direct target of miR-802. P27 elevation counteracted the promotion effect of OS on EMT, migration and invasion induced by miR-802. In addition, miR-802 overexpression inactivated PI3K/AKT pathway via targeting p27 in OS.ConclusionMiR-802 promoted the progress of EMT, migration and invasion in OS via targeting p27. This newly identified miR-802/p27/PI3K/AKT axis may represent potential targets for OS.

The novel circ_0084904/miR-802/MAL2 axis promotes the development of cervical cancer.

Circular RNAs (circRNAs) have been identified as critical regulators in human cancers, including cervical cancer (CC). However, the precise action of circ_0084904 in cervical carcinogenesis remains to be elucidated. The levels of circ_0084904, microRNA (miR)-802, and Mal, T cell differentiation protein 2 (MAL2) were checked by quantitative real-time PCR (qRT-PCR) or western blot. Ribonuclease R (RNase R) and subcellular localization assays were used to detect the stability and localization of circ_0084904, respectively. Cell colony formation ability was assessed by colony formation assay. Cell cycle and apoptosis were detected by flow cytometry. Cell migration and invasion abilities were gauged by transwell assay. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were applied to determine the direct relationship between miR-802 and circ_0084904 or MAL2. The xenograft experiments were performed to evaluate the role of circ_0084904 in tumor growth in vivo. Circ_0084904 was markedly up-regulated in CC tissues and cell lines. Silencing endogenous circ_0084904 impeded cell colony formation, cell cycle progression, migration, invasion, epithelial-mesenchymal transition (EMT), and promoted apoptosis in vitro, as well as diminished tumor growth in vivo. Mechanistically, circ_0084904 targeted miR-802, and the effects of circ_0084904 silencing were mediated by miR-802. MAL2 was directly targeted and inhibited by miR-802, and MAL2 was a functional target of miR-802. Moreover, circ_0084904 modulated MAL2 expression via miR-802. Our study identified circ_0084904 as a novel oncogenic driver in CC depending on the modulation of the miR-802/MAL2 axis, establishing the notion that silencing of circ_0084904 might represent a promising targeted therapy for CC.

MicroRNA-802 promotes the progression of osteosarcoma through targeting p27 and activating PI3K/AKT pathway.

PURPOSE: Increasing evidences suggest dysfunctions of microRNAs (miRNAs) are playing important part in tumors. Therefore, the role of miR-802 in osteosarcoma (OS) was exploited. The object was to evaluate the effect of miR-802 and verify its influence on p27 Kip1 (p27) in OS. METHODS: RT-qPCR experiment was used to detect miR-802 and p27 expression in OS tissues and cells. We explored the function of miR-802 through Transwell assays. The phosphoinositide 3-kinase (PI3K)/AKT serine/threonine kinase pathway and epithelial-mesenchymal transition (EMT) was detected by Western blot assays. Luciferase assay was used to testify the target of miR-802. RESULTS: MiR-802 expression was elevated in OS, which was related to poor clinical outcome in OS patients. MiR-802 overexpression promoted OS migration, invasion and EMT. Further, p27 is a direct target of miR-802. P27 elevation counteracted the promotion effect of OS on EMT, migration and invasion induced by miR-802. In addition, miR-802 overexpression inactivated PI3K/AKT pathway via targeting p27 in OS. CONCLUSION: MiR-802 promoted the progress of EMT, migration and invasion in OS via targeting p27. This newly identified miR-802/p27/PI3K/AKT axis may represent potential targets for OS.

Dysfunction of miR-802 in tumors.

Recent studies have shown that miR-802 is abnormally expressed in many tumors. miR-802 is expressed at low levels in tissues and cells of gastric cancer, colorectal cancer, breast cancer, cervical cancer, epithelial ovarian cancer, tongue squamous cell carcinoma, oral squamous cell carcinoma, esophageal squamous cell carcinoma, laryngeal squamous cell carcinoma, and melanoma. In contrast, miR-802 is overexpressed in hepatocellular carcinoma, bladder urothelial cancer, osteosarcoma, and cholesteatoma tissue cells. It should be noted that the results of studies on the expression of miR-802 in pancreatic cancer, prostate cancer, and lung cancer are inconsistent. Current studies have found that miR-802 can target and regulate genes in different tumors, and affect the regulation of the Wnt signaling pathway, EMT signaling pathway, PI3K/AKT signaling pathway, ERK signaling pathway, and Hedgehog signaling pathway. At the same time, miR-802 is regulated by the endogenous competition of four ceRNAs, including circDONSON, IGFL2-AS1, MIR155HG, and MIR4435-2HG. This article reviews the abnormal expression of miR-802 in a variety of tumors, expounds the mechanism by which miR-802 affects tumor progression by regulating different target genes, and elaborates the network of miR-802-related ceRNAs. We also summarized the limitations of miR-802 research and looked forward to the potential application of miR-802 in the diagnosis and prognosis of tumors.

Therapeutic inhibition of miR-802 protects against obesity through AMPK-mediated regulation of hepatic lipid metabolism.

Background: The host-parasite relationship is based on subtle interplay between parasite survival strategies and host defense mechanisms. It is well known that helminth infection, which afflicts more than one billion people globally, correlates with a decreased prevalence of obesity. Dissecting the underlying mechanisms can provide new targets for treating obesity from the host-parasite interaction perspective. Methods: C57BL/6 mice received a normal or high-fat diet (HFD) with or without Sjp40 (one main component of schistosome-derived soluble egg antigens) treatment. Both the loss and gain-of-function experiments by the inhibitor suppression and lentivirus treatment of miR-802 were utilized to elucidate the role of miR-802/AMPK axis in host lipid metabolism. Hepatocyte lipogenesis assay and metabolic parameters were assessed both in vivo and in vitro. The potential interactions among Sjp40, CD36, miR-802, Prkab1, and AMPK were clarified by pull-down, miRNA expression microarray, quantitative RT-PCR, dual-luciferase reporter assay, and western blotting analysis. Results: We showed a link between decreased miR-802 and impaired lipid metabolism in Schistosoma japonicum infected mice. The decreased miR-802 promotes murine Prkab1 or human Prkaa1 expression, respectively, which increases levels of phosphorylated AMPK, resulting in a decrease in hepatic lipogenesis. Also, injection with schistosome-derived soluble egg antigens (SEA) attenuated metabolism. We demonstrated that Sjp40 as a main component of SEA interacted with CD36 on hepatocytes to inhibit miR-802, resulting in the activation of AMPK pathway and subsequent attenuation of lipogenesis. Collectively: Our study reveals the significant role of miR-802/AMPK axis in hepatic lipid metabolism and identifies the therapeutic potential of Sjp40 in treating obesity-related fatty liver.

Identification of MYLIP gene and miRNA-802 involved in the growth and metastasis of cervical cancer cells.

BACKGROUND: The dysregulation of microRNA-802 (miR-802) has crucial roles in cancer progression. Nevertheless, the bio-function of miR-802 in cervical cancer remains unclear. OBJECTIVE: Hence, we illuminated the potential roles of miR-802 in cervical cancer cell growth, migration, and invasion. METHODS: The levels of miR-802 and myosin regulatory light chain interacting protein (MYLIP) were measured using qRT-PCR assay. The potential effects of miRNA-802 on cervical cancer cell proliferation and metastatic phenotypes were determined using CCK-8, colony formation, wound healing and Transwell invasion assays. MYLIP was validated as a downstream target gene of miRNA-802 using bioinformatics analysis tool and luciferase report gene assay. The impact of miR-802 on the growth of cervical cancer cell in vivo was analyzed using xenograft model. The expression of MYLIP was measured by western blotting and immunohistochemistry (IHC). RESULTS: MiRNA-802 was distinctly down-regulated in cervical cancer cells as well as clinical cervical cancer samples. Upregulation of miRNA-802 significantly inhibited the growth and aggressiveness of cervical cancer cell. Additional, MYLIP was a functional target of miR-802. MYLIP was ovrerexpressed in cervical cancer and MYLIP level was negatively associated with the level of miR-802. Overexpression of MYLIP eliminated the inhibitory effects of miR-802 on growth and metastatic-related traits of cervical cancer cell. In vivo, miR-802 also markedly reduced the tumor growth of cervical cancer cell and decreased the expression of MYLIP. CONCLUSIONS: MiR-802 inhibits the growth and metastatic-related phenotypes of cervical cancer cell through targeting MYLIP.

MicroRNA-802 Suppresses Tumorigenesis of Colorectal Cancer via Regulating UBN2.

BACKGROUND: The initiation and progression of colorectal cancer (CRC) are a multistep complex process regulated by multiple factors. Previous evidence indicated that microRNA-802 (miR-802) participated in tumorigenesis of numerous solid cancers; however, the potential roles and underlying mechanisms of miR­802 in CRC still need further exploration. METHODS: Quantitative real-time PCR (qRT-PCR) was employed to evaluate miR-802 levels in human CRC tissues and cell lines. In vitro proliferation, apoptosis, migration and invasion assays, and in vivo subcutaneous mouse xenograft model were utilized to examine the effects of miR-802 on the malignant behaviors of CRC cells. Then, bioinformatics prediction, dual-luciferase reporter, qRT-PCR, and Western blot was conducted to confirm the down-stream target of miR-802. RESULTS: MiR-802 was frequently down-regulated in CRC tissues and cells. Further analyses showed that the low expression of miR-802 in CRC tissues was significantly correlated with tumor progression and poor patients' prognosis. Overexpression of miR-802 profoundly inhibited proliferation, migration and invasion but promoted apoptosis of CRC cells, by contrast, miR-802 silencing exhibited opposite effects in vitro. Further animal experiment demonstrated that miR-802 could suppress tumor growth via inhibiting the proliferation and promoting the apoptosis of CRC cells in vivo. Mechanistically, miR-802 functioned as a tumor suppressor through inhibiting the expression of Ubinuclein-2 (UBN2) on post-transcriptional level. Moreover, upregulation of UBN2 expression could reverse the biological effects of CRC cells induced by miR-802 overexpression. CONCLUSION: Our study demonstrates that miR-802 inhibits the proliferation, migration and invasion while promotes the apoptosis of CRC cells via directly suppressing UBN2 expression. These findings provide a promising biomarker and potential treatment target for CRC.

ZNF521 which is downregulated by miR-802 suppresses malignant progression of Hepatocellular Carcinoma through regulating Runx2 expression.

Zinc finger protein 521 (ZNF521) plays an important role in the tumor development and process. However, its regulatory role in hepatocellular carcinoma (HCC) remains unclear. In this study, we demonstrated for the first time that ZNF521 mRNA and protein was down-regulated in HCC tissues and cell lines. Down-regulated ZNF521 expression was significantly associated with malignant prognostic features, including advanced TNM stage and large tumor size. For 5-year survival, ZNF521 served as a potential prognostic marker of HCC patients. Moreover, ZNF521 inhibited cell proliferation, colony formation and cell viability through Runx2 transcriptional inhibition and AKT phosphorylation pathway. Moreover, we demonstrated that ZNF521 expression was regulated by miR-802. In HCC tissues. MiR-802 has an inverse correlation with ZNF521 expression. In conclusion, we demonstrate for the first time that ZNF521 is down-regulated in HCC tissues and inhibits HCC growth through Runx2 transcriptional inhibition and AKT inactivation, which was regulated by miR-802, suggesting the potential therapeutic value for HCC.

CircRNA DONSON contributes to cisplatin resistance in gastric cancer cells by regulating miR-802/BMI1 axis.

BACKGROUND: Circular RNA downstream neighbor of SON (circDONSON) has been revealed to promote gastric cancer (GC) growth and invasion, while the role and molecular mechanism underlying circDONSON in GC cisplatin (DDP) resistance remain unclear. METHODS: Levels of circDONSON, microRNA (miR)-802, and B lymphoma Mo-MLV insertion region 1 (BMI1) mRNA were detected using quantitative real-time polymerase chain reaction. Cell viability and apoptosis were measured by cell counting kit-8 assay, colony formation assay and flow cytometry, respectively. Protein levels of BMI1, Cyclin D1, p27, Caspase-3 Cleavage and Caspase-9 Cleavage were determined by western blot. The interaction between miR-802 and circDONSON or BMI1 was confirmed by dual-luciferase reporter assay. In vivo experiments were conducted via the murine xenograft model. RESULTS: CircDONSON was elevated in GC tissues and cell lines, especially in DDP-resistant GC tissues and cells. Knockdown of circDONSON sensitized GC cells to DDP by inhibiting cell viability and promoting cell apoptosis in vitro. Further mechanism-related investigations suggested that circDONSON functioned as "sponge" by competing for miR-802 binding to modulate its target BMI1. Silencing miR-802 reversed the inhibition of DDP-resistance in GC cells induced by circDONSON down-regulation. Besides, miR-802 alleviated DDP resistance in GC cells by targeting BMI1. Functionally, circDONSON knockdown enhanced the cytotoxicity of DDP in GC in vivo. CONCLUSION: Our findings demonstrated circDONSON promoted cisplatin resistance in gastric cancer cells by regulating miR-802/BMI1 axis, shedding light on the development of a novel therapeutic strategy to overcome chemoresistance in gastric cancer patients.

MiR-802 Suppresses Colorectal Cancer Cell Viability, Migration and Invasion by Targeting RAN.

PURPOSE: Colorectal cancer is one of the most malignant tumors in the world, and the incidence is increasing every year. MicroRNAs (miRNA) are small non-coding RNAs that are involved in a variety of physiological or pathological processes. Abnormal expression of microRNA-802 (miR-802) has been demonstrated in various types of cancer. However, the expression and biological role of miR-802 in human colorectal cancer remain largely unknown. METHODS: Here, we used quantitative real-time PCR (qRT-PCR) to measure miR-802 expression levels in colorectal cancer tissues and cell lines. Cell Counting Kit-8 (CCK-8) was used to assess the effect of miR-802 on colorectal cancer cell viability. Migration and invasion assays were performed to determine the effect of miR-802 on metastasis of colon tumor cells by transwell analysis. Luciferase activity assays were used to confirm the target of miR-802. RESULTS: The results show that miR-802 is significantly downregulated in colorectal cancer tissues and cell lines. Overexpression of miR-802 profoundly inhibited viability, migration and invasion of colorectal cancer cells. In addition, we have newly discovered that the Ras-associated nucleus (RAN) is a direct target of miR-802 which could reverse the effects induced by miR-802 overexpression in colorectal cancer cells. CONCLUSION: In conclusion, our study shows that miR-802 is downregulated in colorectal cancer, and overexpression of miR-802 inhibits colorectal cancer cell viability, migration and invasion by directly targeting RAN.

miR-802 participates in the inflammatory process of inflammatory bowel disease by suppressing SOCS5.

The present study aims to reveal the detailed molecular mechanism of microRNA (miR)-802 in the progression of inflammatory bowel disease (IBD). IBD tissues were obtained from IBD patients, followed by CD4+ cells isolation. Then, qRT-PCR and ELISA were used to detect the expression of miR-802, suppressor of cytokine signaling 5 (SOCS5), interleukin (IL)-17A and tumor necrosis factor (TNF)-α. Transfection of miR-802 mimics and miR-802 inhibitor in CD4+ cells was detected by Western blot. TargetScan and luciferase reporter assay were used to detect the relationship between SOCS5 and miR-802. Finally, colitis mice model was established to verify whether miR-802 inhibitor was involved in the protective effect of colonic mucosa. The miR-802 was highly expressed in inflamed mucosa and PBMC cells of IBD. The highest expression of miR-802 was observed in CD4+ T cells based on different immune cell subsets analysis. SOCS5 was the target gene of miR-802. The mice model experiments showed that blockade of miR-802 could alleviate mice colitis. Our study suggests that up-regulation of miR-802 plays an important role in inflammatory process of IBD via targeting SOCS5. Moreover, the differentiation of Th17 and secretion of TNF-α in IBD could be stimulated by miR-802.

MicroRNA-802 Inhibits Cell Proliferation and Induces Apoptosis in Human Laryngeal Cancer by Targeting cAMP-Regulated Phosphoprotein 19.

BACKGROUND/AIMS: miR-802 plays a key role in cancer progression and development. The purpose of this work is to investigate the functional role of miR-802 in laryngeal cancer and to elucidate the function of miR-802 and cAMP-regulated phosphoprotein 19 (ARPP19) on laryngeal cancer. METHODS: RT-qPCR was applied to study the expression level of ARPP19 and miR-802 in the laryngeal carcinoma cell lines and tissues. CCK-8, colony formation, flow cytometry (FACS) assay were used to study the effect of ARPP19 and miR-802 on apoptosis, proliferation, and cell cycle of laryngeal carcinoma cells. Target gene prediction and luciferase reporter gene assay were applied to identify target gene of miR-802. The transcriptional mRNA and protein expression levels of ARPP19 were measured by RT-qPCR or Western blotting. RESULTS: miR-802 was down-regulated in laryngeal carcinoma cell lines and tissues. Laryngeal cancer cells transfected by miR-802 mimic were significantly inhibited in the terms of cell colony formation and proliferation. Furthermore, miR-802 can inhibit the expression level of ARPP19 by directly targeting the 3' untranslated region (3'-UTR) of ARPP19. Overexpression of the ARPP19 gene can reverse the suppressive effect of miR-802 on laryngeal cancer cells. CONCLUSION: miR-802 can exert tumor suppressor effects in laryngeal carcinoma by targeting ARPP19, indicating that miR-802 protein may play a role of potential therapeutic target for clinical laryngeal cancer.

LncRNA IGFL2-AS1 functions as a ceRNA in regulating ARPP19 through competitive binding to miR-802 in gastric cancer.

Gastric cancer (GC) is one of the most common malignancies of the digestive system worldwide. Multiple long noncoding RNAs (lncRNAs) participate in the regulation of GC development and metastasis. In this study, we aimed to elucidate the expression and function of lncRNA IGFL2-AS1 in GC. We found that IGFL2-AS1 was highly expressed in GC tissues and cell lines. Knockdown of IGFL2-AS1 suppressed GC cell proliferation, migration, and invasion in vitro. Furthermore, we identified that IGFL2-AS1 exerted its function as a molecular sponge of miR-802. MiR-802 was demonstrated to be a tumor suppressor, and overexpression of miR-802 suppressed GC cell growth, migration, and invasion. Mechanistically, we revealed that the cAMP-regulated phosphoprotein 19 (ARPP19) was a direct target of miR-802 and could reverse the inhibitory function of miR-802. Moreover, our results confirmed that knockdown of IGFL2-AS1 inhibited GC tumor development in an in vivo GC tumor xenograft model. In summary, our data suggest that the IGFL2-AS1/miR-802/ARPP19 axis plays a critical role in the progression and metastasis of GC. Therapies targeting the IGFL2-AS1/miR-802/ARPP19 axis can potentially improve GC treatment.

Identification of miR-802-5p and its involvement in type 2 diabetes mellitus.

MicroRNAs (miRNA) are recently discovered endogenous, small noncoding RNAs (of 22 nucleotides) that play pivotal roles in gene regulation. They are involved in post-transcriptional control of gene expression. miRNAs are emerging as important regulators of cell proliferation, development, cancer formation, stress responses, cell death and physiological conditions. Increasing evidence has demonstrated the human miRNAs bind to their target mRNA sequences with perfect or near-perfect sequence complementarily. This provides a powerful strategy for discovering potential type 2 diabetes mellitus (T2DM) targets and gives the probability to exploit them for diagnostic and therapeutic causes. About 6% of the world population is affected by T2DM, and it is recognized as a global epidemic by the World Health Organization. At present there is no valid biomarker to control or manage T2DM. Therefore, the present study applied a mature sequence of miRNAs from publicly accessible databases to identify the miRNA from T2DM expressed sequence tags, and the results are detailed and discussed below.

MiR-802 alleviates lipopolysaccharide-induced acute lung injury by targeting Peli2.

INTRODUCTION: Acute respiratory distress syndrome (ARDS) is a life-threatening medical condition. It is characterized by serious lung inflammation or injury. Characterizing novel miRNAs implicated in ARDS pathogenesis may provide new therapeutic strategy for managing ARDS. METHODS: We employed LPS-induced lung injury model to profile miRNAs associated with ARDS. We isolated one miRNA candidate and characterized its role in lipopolysaccharide (LPS)-induced proinflammatory cytokine production in lung macrophages. We further evaluated its functional role in ARDS model by assessing histological change, neutrophil activation, tissue permeability and tumor necrosis factor alpha (TNFα) production. We also characterized its downstream target using luciferase assay, Western blotting, enzyme-linked immunosorbent assay and cell inflammation assay. RESULTS: Microarray profiling revealed miR-802 was significantly downregulated in ARDS mouse model. LPS-induced miR-802 downregulation was confirmed in lung macrophages. Overexpression of miR-802 significantly suppressed LPS-induced inflammatory cytokine production in vitro and alleviates LPS-induced acute lung injury in vivo. Peli2 was identified as a downstream target of miR-802 and found upregulated in ARDS model. Overexpressing Peli2 abolished the antagonizing effect of miR-802 on LPS-mediated inflammatory response. CONCLUSION: MiR-802 carried a protective role against LPS-induced acute lung injury by downregulating Peli2. MiR-802/Peli2 axis may act as intervening targets to manage ARDS.