Upregulation of microRNA-27b contributes to the migration and invasion of gastric cancer cells via the inhibition of sprouty2-mediated ERK signaling

Jiang, Juan; Yi, Bo; Qin, Chunxiang; Cao, Wei

doi:10.3892/mmr.2016.4779

Cited by 6 publications

(5 citation statements)

References 28 publications

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“…This data indicated that miR-23a was able to activate the ERK signaling via the inhibition of SPRY2, and thus promote the malignant phenotypes of AGS cells. Similarly, a previous study also indicated that miR-27a was able to promote the migration and invasion of gastric cancer cells via inhibiting the expression of SPRY2, and thus activating ERK signaling ( 32 ).…”

Section: Discussionmentioning

confidence: 69%

microRNA‑23a promotes cell growth and metastasis in gastric cancer via targeting SPRY2‑mediated ERK signaling

Chen

She

et al. 2018

Oncol Lett

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microRNAs (miRs) serve important roles in various human cancer types. Recently, miR-23a has been indicated as an oncogene in gastric cancer, but the underlying mechanism remains unclear. In the present study, reverse transcription-quantitative polymerase chain reaction and western blot analysis was used to explore the effects of miR-23a in gastric cancer. Additionally, cell proliferation, migration and invasion were examined using an MTT assay, wound healing assay and Transwell assay, respectively. Furthermore, a luciferase reporter gene assay was used to confirm the target association. It was determined that miR-23a was significantly upregulated in gastric cancer tissues and cell lines compared with adjacent tissues, and a normal gastric epithelial cell line. Furthermore, its upregulation was significantly associated with cancer progression and poor prognosis of patients. Knockdown of miR-23a caused a notable reduction in the proliferation, migration and invasion of gastric cancer AGS cells. Sprouty homolog 2 (SPRY2) was then predicted to be target gene of miR-23a. A luciferase reporter gene assay data demonstrated that miR-23a has the ability to directly bind to the 3′-untranslational region of SPRY2 mRNA. Further investigation demonstrated that SPRY2 was significantly downregulated in gastric cancer tissues and cell lines, and the protein expression of SPRY2 was negatively regulated by miR-23a in AGS cells. Furthermore, knockdown of SPRY2 reduced the suppressive effects of miR-23a inhibition in AGS cell proliferation, migration and invasion. In addition, the activity of extracellular signal-regulated kinase (ERK) signaling was also inhibited by the miR-23a/SPRY2 knockdown in AGS cells. The present study indicated that miR-23a serves a promoting role in gastric cancer via targeting SPRY2 and downstream ERK signaling.

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Section: Discussionmentioning

confidence: 69%

microRNA‑23a promotes cell growth and metastasis in gastric cancer via targeting SPRY2‑mediated ERK signaling

Chen

She

et al. 2018

Oncol Lett

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“…Mechanistically, miR-1323 promoted the migration of lung cancer cells by targeting Cbl-b. It is well-known that microRNAs are involved in multiple biological processes such as cell differentiation, proliferation, apoptosis, EMT, and cell migration, through targeting gene expression (21)(22)(23). Previously, a study has shown that miR-1323 promoted radiation-resistant lung cancer cells (10).…”

Section: Discussionmentioning

confidence: 99%

miR-1323 Promotes Cell Migration in Lung Adenocarcinoma by Targeting Cbl-b and Is an Early Prognostic Biomarker

et al. 2020

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Purpose: MicroRNAs are known to regulate cellular processes in non-small cell lung cancer (NSCLC) cells and predict prognosis. However, identification of specific microRNAs in NSCLC as potential therapeutic targets is controversial. We aim to determine the clinical significance of miR-1323 in the prognosis of patients with lung cancer and the potential mechanism. Patients and methods: A bioinformatics approach was used to screen the importance microRNA in NSCLC through the online GEO database (GSE42425). The relationship between expression level of miR-1323 and overall survival of lung cancer patients was analyzed. Additionally, an independent corhort including 53 NSCLC cases that underwent resection validated the connection between miR-1323 and LUAD patients' overall survival. Next, the function of miR-1323 was studied in vitro by transient transfection. A more in-depth mechanism was studied through luciferase reporter gene experiments. Results: High miR-1323 expression correlated with poor survival in NSCLC patients (P = 0.011), and in lung adenocarcinoma (LUAD) patients (P = 0.015) based on GEO database (GSE42425). In the independent cohort based on our hospital, high miR-1323 expression was associated with LUAD patients (P = 0.025). Moreover, transfection with mimics of miR-1323 showed an increased migratory capacity in LUAD A549 and HCC827 cells. In addition, E3 ubiquitin-protein ligase Casitas B-lineage Lymphoma-b (Cbl-b) was found to be the target genes of miR-1323 and significantly down regulated after mimics of miR-1323 transfection, and high Cbl-b expression predicted better prognosis in NSCLC and LUAD (P = 0.00072 and P = 0.02, respectively). Conclusion: The miR-1323 promoted LUAD migration through inhibiting Cbl-b expression. High miR-1323 expression predicted poor prognosis in LUAD patients.

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“…Except for regulating EMT, miRNA-27b plays a vital role in the transfer via inhibiting multiple genes that are associated with motility and migration at the post-transcriptional level. SPRY2-mediated ERK signaling activation may be another mechanism for miR-27b inducing the invasion and of migration of GC cells proved by Jiang et al 57 MiR-27b is decreased in metastatic, castration-resistant PCa tissue and cells, and suppresses migration and invasion which are key metastatic processes in PCa cells ALVA31 and PC3-ML. These inhibitory effects on migration and invasion are concomitant with decreased activity of Rac1 without affecting total Rac1 levels and enhanced level of tumor suppressor E-cadherin.…”

Section: Introductionmentioning

confidence: 94%

Promising therapeutic role of miR-27b in tumor

Ding

Yang

et al. 2017

Tumour Biol.

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MicroRNAs are small nonprotein-encoding RNAs ranging from 18 to 25 nucleotides in size and regulate multiple biological pathways via directly targeting a variety of associated genes in cancers. MicroRNA-27b is a highly conserved MicroRNA throughout vertebrates and there are two homologs (hsa-miR-27a and hsa-miR-27b) in humans. MicroRNA27b is an intragenic microRNA located on chromosome 9q22.1 within the C9orf3 gene, clustering with miR-23b and miR-24-1 in human. As a frequently dysregulated microRNA in human cancers, microRNA-27b could function as a tumor suppressor or an oncogenic microRNA. More and more studies indicate that microRNA-27b is involved in affecting various biological processes, such as angiogenesis, proliferation, metastasis, and drug resistance, and thus may act as a promising therapeutic target in human cancers. In this review, we discuss the role of microRNA-27b in detail and offer novel insights into molecular targeting therapy for cancers.

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Upregulation of microRNA-27b contributes to the migration and invasion of gastric cancer cells via the inhibition of sprouty2-mediated ERK signaling

Cited by 6 publications

References 28 publications

microRNA‑23a promotes cell growth and metastasis in gastric cancer via targeting SPRY2‑mediated ERK signaling

microRNA‑23a promotes cell growth and metastasis in gastric cancer via targeting SPRY2‑mediated ERK signaling

miR-1323 Promotes Cell Migration in Lung Adenocarcinoma by Targeting Cbl-b and Is an Early Prognostic Biomarker

Promising therapeutic role of miR-27b in tumor

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