Upregulation of microRNA-31 targeting integrin α5 suppresses tumor cell invasion and metastasis by indirectly regulating PI3K/AKT pathway in human gastric cancer SGC7901 cells

Zhang, Xuebin; Song, Lei; Wen, Hongjuan; Bai, Xiaoxue; Li, Zhen-Juan; Ma, Lu‐Fang

doi:10.1007/s13277-015-4511-y

Cited by 30 publications

(29 citation statements)

References 26 publications

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“…These results were in accordance with the study conducted by Xie et al [20] who found that ITGA5 could promote growth, migration, and invasion of esophageal squamous cell carcinoma (ESCC) cells. However, we also found that multiple miRNAs (except miR-330-5p) could also target ITGA5, including miR-128, miR-31, miR-26a, and miR-205 [23,25,33,34]. Several other factors could modulate the expression of ITGA5 as well.…”

Section: Discussionmentioning

confidence: 80%

“…Several previous studies have indicated that ITGA5 can operate in certain cancers—including breast cancer, non-small cancer, and gastric cancer—by activating focal adhesion kinase to promote cell adhesion and migration [20,22–24]. For example, Zhang et al [25] found that ITGA5 can work with miR-31 in affecting cell invasion and metastasis of gastric cancer. Although ITGA5 has been studied in several different malignancies, few researches have been conducted to evaluate its function and expression level in GBM.…”

Section: Introductionmentioning

confidence: 99%

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miR-330-5p suppresses glioblastoma cell proliferation and invasiveness through targeting ITGA5

Feng

et al. 2017

Bioscience Reports

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The present study intended to investigate the biological effects of miR-330-5p on glioblastoma (GBM) cell proliferation and invasiveness by targeting integrin α5 (ITGA5). The expressions of miR-330-5p and ITGA5 mRNA in GBM cell lines (U87, U251, and U373) and normal brain glial cell line (HEB) were detected using RT-qPCR. Protein expression of ITGA5 was examined using Western blot. The present study used MTT assay, colony formation assay, Transwell assay, wound healing assay, and flow cytometry analysis in order to determine the biological functions of GBM cells (including cell proliferation, invasion, migration, apoptosis, and cell cycle). The present study applied dual-luciferase reporter gene assay to identify the target relationship between miR-330-5p and ITGA5. miR-330-5p was low-expressed in GBM cell lines while ITGA5 was high-expressed compared with HEB. miR-330-5p could directly target ITGA5 as well as suppress its expression in GBM cells. Up-regulation of miR-330-5p and down-regulation of ITGA5 both have an inhibitory effect on cell proliferation, invasion, and migration. Meanwhile, they could also promote GBM cell apoptosis. miR-330-5p could suppress proliferation and invasion of GBM cells through targeting ITGA5.

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Section: Discussionmentioning

confidence: 80%

Section: Introductionmentioning

confidence: 99%

miR-330-5p suppresses glioblastoma cell proliferation and invasiveness through targeting ITGA5

Feng

et al. 2017

Bioscience Reports

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“…When considering all 37 infection-regulated miRNAs whose expression differed between the two mouse strains, nine miRNAs had targets that were significantly over-represented in the PI3K-Akt signaling pathway (DIANA tool). Five of these [miR-34b-3p, miR-34c-5p, miR-34b-5p, miR-92b-3p, and miR-182-5p; as well as miR-31-5p, which was identified through literature search (41)] belonged to the aforementioned seven miRNAs which were expressed more highly in the C57BL/6J mice and downregulated throughout the time course.…”

Section: Resultsmentioning

confidence: 99%

Host Genetic Background Strongly Affects Pulmonary microRNA Expression before and during Influenza A Virus Infection

2017

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BackgroundExpression of host microRNAs (miRNAs) changes markedly during influenza A virus (IAV) infection of natural and adaptive hosts, but their role in genetically determined host susceptibility to IAV infection has not been explored. We, therefore, compared pulmonary miRNA expression during IAV infection in two inbred mouse strains with differential susceptibility to IAV infection.ResultsmiRNA expression profiles were determined in lungs of the more susceptible strain DBA/2J and the less susceptible strain C57BL/6J within 120 h post infection (hpi) with IAV (H1N1) PR8. Even the miRNomes of uninfected lungs differed substantially between the two strains. After a period of relative quiescence, major miRNome reprogramming was detected in both strains by 48 hpi and increased through 120 hpi. Distinct groups of miRNAs regulated by IAV infection could be defined: (1) miRNAs (n = 39) whose expression correlated with hemagglutinin (HA) mRNA expression and represented the general response to IAV infection independent of host genetic background; (2) miRNAs (n = 20) whose expression correlated with HA mRNA expression but differed between the two strains; and (3) remarkably, miR-147-3p, miR-208b-3p, miR-3096a-5p, miR-3069b-3p, and the miR-467 family, whose abundance even in uninfected lungs differentiated nearly perfectly (area under the ROC curve > 0.99) between the two strains throughout the time course, suggesting a particularly strong association with the differential susceptibility of the two mouse strains. Expression of subsets of miRNAs correlated significantly with peripheral blood granulocyte and monocyte numbers, particularly in DBA/2J mice; miR-223-3p, miR-142-3p, and miR-20b-5p correlated most positively with these cell types in both mouse strains. Higher abundance of antiapoptotic (e.g., miR-467 family) and lower abundance of proapoptotic miRNAs (e.g., miR-34 family) and those regulating the PI3K-Akt pathway (e.g., miR-31-5p) were associated with the more susceptible DBA/2J strain.ConclusionSubstantial differences in pulmonary miRNA expression between the two differentially susceptible mouse strains were evident even before infection, but evolved further throughout infection and could in part be attributed to differences in peripheral blood leukocyte populations. Thus, pulmonary miRNA expression both before and during IAV infection is in part determined genetically and contributes to susceptibility to IAV infection in this murine host, and likely in humans.

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“…In gliomas, ADAMTS9-AS2 acts as a novel tumor suppressor that inhibits glioma cell metastasis. [25][26][27] The PI3K-Akt signaling pathway is involved in important functions such as growth, differentiation, invasion, and metastasis of gastric cancer cells. 23 In ovarian cancer, ADAMTS9-AS2 affects the progression of ovarian cancer by targeting the miR-182-5p/FOXF2 signaling pathway.…”

Section: Relationship Between Lncrnamentioning

confidence: 99%

Identification of the complex regulatory relationships related to gastric cancer from lncRNA‐miRNA‐mRNA network

Wang

Ding

et al. 2019

J of Cellular Biochemistry

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The oncogenesis and progression of gastric cancer are closely correlated with the complex regulatory relationships among messenger RNA (mRNA), long noncoding RNA (lncRNA), and microRNA (miRNA). After constructing the gastric cancer lncRNA‐miRNA‐mRNA regulatory network, we analyzed the network topology properties and found that lncRNA ADAMTS9‐AS2 and C20orf166‐AS1 and miRNA hsa‐mir‐204 are key nodes. Further functional enrichment analysis and survival analysis were performed on these key nodes and the RNAs interacting with them. We found that CHRM2, ANGPT2, and COL1A1 interacting with ADAMTS9‐AS2 are enriched in the PI3K‐Akt signaling pathway, and low expression of the ADAMTS9‐AS2 is closely related to the prognosis of patients. Abnormal expression of CACNA1H, FLNA, and FLNC interacting with lncRNA C20orf166‐AS1 is associated with MAPK signaling pathway in gastric cancer. In addition, the downregulated miRNA hsa‐mir‐204 promotes invasion and proliferation of gastric cancer cells by regulating the abnormal expression of mRNAs (CHRDL1 and NPTX1) and lncRNAs (ADAMTS9‐AS2, NKX2‐1‐AS1, TLR8‐AS1, and VCAN‐AS1). This study systematically analyzed the lncRNA‐miRNA‐mRNA regulatory network of gastric cancer, which not only has a new understanding of the pathogenesis of gastric cancer, but also provides new insights for the early diagnosis and treatment of gastric cancer.

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Upregulation of microRNA-31 targeting integrin α5 suppresses tumor cell invasion and metastasis by indirectly regulating PI3K/AKT pathway in human gastric cancer SGC7901 cells

Cited by 30 publications

References 26 publications

miR-330-5p suppresses glioblastoma cell proliferation and invasiveness through targeting ITGA5

miR-330-5p suppresses glioblastoma cell proliferation and invasiveness through targeting ITGA5

Host Genetic Background Strongly Affects Pulmonary microRNA Expression before and during Influenza A Virus Infection

Identification of the complex regulatory relationships related to gastric cancer from lncRNA‐miRNA‐mRNA network

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