Hsa-miR-875-5p exerts tumor suppressor function through down-regulation of EGFR in colorectal carcinoma (CRC)

Zhang, Tie-Ning; Cai, Xueli; Li, Qi; Xue, Peng; Chen, Zhixiao; Dong, Xiao; Xue, Ying

doi:10.18632/oncotarget.9944

Cited by 29 publications

(27 citation statements)

References 47 publications

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“…To explore whether GACAT1 also functioned as a miRNA sponge, we performed prediction analysis and found that microRNA-875-3p may be a potential target for GACAT1. Previous studies have shown that microRNA-875-3p plays a role as a tumor suppressor gene in a variety of tumors, and its upregulation can often inhibit the proliferation and invasion of tumor cells (18,19). Therefore, we also examined the level of microRNA-875-3p in breast cancer patients, and the results showed that microRNA-875-3p was conspicuously under-expressed in breast cancer.…”

Section: Discussionmentioning

confidence: 94%

Long-chain non-coding RNA GACAT1 promotes development and progression of breast cancer by targeting microRNA-875-3p

et al. 2020

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Role of long-chain non-coding ribonucleic acid (lncRNA) GACAT1 in the development of breast cancer and its possible mechanism were investigated. The levels of GACAT1, microRNA-875-3p and Stonin2 (STON2) in breast cancer tissues and adjacent normal tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The level of GACAT1 in breast cancer cell lines was further explored. The effects of GACAT1 and microRNA-875-3p on cell proliferation and cycle were detected by cell counting kit-8 (CCK-8) and flow cytometry. The binding relationship between microRNA-875-3p and STON2, microRNA-875-3p and GACAT1 was examined by a dual luciferase reporting assay. It was confirmed by rescue experiments whether GACAT1 canregulate the level of STON2 by binding to microRNA-875-3p. GACAT1 level was clearly enhanced in breast cancer tissues compared to that of the adjacent tissues. Similar result was observed in breast cancer cell lines. Upregulation of GACAT1 promoted the proliferation and cycle of breast cancer cells including MCF-7 and BCap-37. The dual luciferase reporting assay results indicated that GACAT1 had a binding relationship with microRNA-875-3p. Further experiments confirmed that microRNA-875-3p was conspicuously downregulated in breast cancer tissues, and upregulation of microRNA-875-3p could inhibit the proliferation ability of MCF-7 and BCap-37 cells, and partially reversed the promoting effect of GACAT1 on cell cycle. Through bioinformatics prediction and dual luciferase reporter gene experiments, we found that STON2 might be a target gene of microRNA-875-3p. Overexpression of STON2 could partially abolish the effect of microRNA-875-3p on cell proliferation and cycle of MCF-7 and BCap-37 cells. GACAT1 can participate in the progression of breast cancer by promoting the proliferation and cycle of breast cancer cells. The mechanism may be through the regulation of the level of STON2 by adsorbing microRNA-875-3p.

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Section: Discussionmentioning

confidence: 94%

Long-chain non-coding RNA GACAT1 promotes development and progression of breast cancer by targeting microRNA-875-3p

et al. 2020

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“…Previous studies have found miR875-5p only in cancer cells, and showed that it promotes cancer cell invasion and epithelial-to-mesenchymal transition [37][38][39] . The present findings revealed expression of miR875-5p in dental mesenchyme, which might be related to the PDGF signaling pathway.…”

Section: Discussionmentioning

confidence: 95%

microRNA-875-5p plays critical role for mesenchymal condensation in epithelial-mesenchymal interaction during tooth development

Funada

Yoshizaki

Miyazaki

et al. 2020

Sci Rep

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Epithelial-mesenchymal interaction has critical roles for organ development including teeth, during which epithelial thickening and mesenchymal condensation are initiated by precise regulation of the signaling pathway. In teeth, neural crest-derived mesenchymal cells expressed PDGF receptors migrate and become condensed toward invaginated epithelium. To identify the molecular mechanism of this interaction, we explored the specific transcriptional start sites (TSSs) of tooth organs using cap analysis of gene expression (CAGE). We identified a tooth specific TSS detected in the chromosome 15qD1 region, which codes microRNA-875 (mir875). MiR875-5p is specifically expressed in dental mesenchyme during the early stage of tooth development. Furthermore, PRRX1/2 binds to the mir875 promoter region and enhances the expression of mir875. To assess the role of miR875-5p in dental mesenchyme, we transfected mimic miR875-5p into mouse dental pulp (mDP) cells, which showed that cell migration toward dental epithelial cells was significantly induced by miR875-5p via the PDGF signaling pathway. Those results also demonstrated that miR875-5p induces cell migration by inhibiting PTEN and STAT1, which are regulated by miR875-5p as part of post-transcriptional regulation. Together, our findings indicate that tooth specific miR875-5p has important roles in cell condensation of mesenchymal cells around invaginated dental epithelium and induction of epithelial-mesenchymal interaction. Tooth morphogenesis, initiated by reciprocal interactions between the ectoderm and neural crest-derived mesenchyme 1-3 , is a good model for understanding the molecular mechanism of epithelial-mesenchymal interaction, because of the well-defined developmental stages and distinctive cell types. In mice, that morphogenesis is initiated by thickening of dental epithelium to form the dental placode, followed by invagination into mesenchyme on embryonic day (E)11.5. In addition, neural crest-derived mesenchymal cells migrate and condense toward the dental epithelial placode. Thereafter, mesenchyme condenses around the epithelial tooth bud and gains an ability for tooth morphogenesis via expression of a particular set of transcription factors and signaling molecules 3,4. During tooth morphogenesis, invaginated epithelium and condensed mesenchymal tissues interact with each other (epithelial-mesenchymal interaction), and form the shape of the tooth. Finally, dental epithelium and mesenchyme differentiate into ameloblasts, which secretes enamel, and odontoblasts, secreting dentin. However, the molecular mechanism of mesenchymal cell migration and condensation have yet to be clearly elucidated. Cranial skeletal tissues including tooth, bone, nerves, and blood vessels are mainly derived from neural crest cells (NCCs) 5-7. The neural crest is composed of transient embryonic tissues present during neural tube formation, whose cells have a high potential for migration and differentiation 7-9. Disruption of cranial NCC migration during embryonic development can lead t...

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“…17 More recently, accumulating investigations into miRs and genes have been conducted, which has drawn increasing attention due to their positive involvements in the progression of human CRC 1,18,19 ; however lack of knowledge still persists focusing on distinct delineation for the combination of miR-98 and CLDN1 in CRC. 17 More recently, accumulating investigations into miRs and genes have been conducted, which has drawn increasing attention due to their positive involvements in the progression of human CRC 1,18,19 ; however lack of knowledge still persists focusing on distinct delineation for the combination of miR-98 and CLDN1 in CRC.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of microRNA‐98 inhibits cell proliferation and promotes cell apoptosis via claudin‐1 in human colorectal carcinoma

Zheng

Luo

Gan

et al. 2018

J of Cellular Biochemistry

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Colorectal carcinoma (CRC) is a major cause of cancer‐related deaths worldwide, and investigations on novel targets are imperative. MiR‐98 has been reported to act as a tumor suppressor in several cancers. To evaluate miR‐98 as a novel anticancer molecule for CRC, examinations to validate whether miR‐98 conferred an inhibiting effect on proliferation, migration, and invasion were performed. The microarray‐based gene expression profiling involving CRC was used to identify the differentially expressed genes. The potential relationship between miR‐98 and CLDN1 was analyzed by cell experimentation. Then, the CRC cells were transfected with miR‐98 mimic or miR‐98 inhibitor to investigate the potential effect of miR‐98 overexpression and depletion on CRC cell proliferation, migration, invasion, and apoptosis. The expressions of CLDN1, Bcl‐2 associated protein x (Bax), runt‐related transcription factor 3 (RUNX3), B‐cell lymphoma 2 (Bcl‐2), C‐myc, and proliferating cell nuclear antigen (PCNA) were determined. The downregulated miR‐98 along with an upregulated CLDN1 was observed in CRC, in which miR‐98 could target to regulate CLDN1. The overexpression of miR‐98 or silencing of CLDN1 was shown to increase the expression of Bax and RUNX3 along with promoted cell apoptosis and arrested cells in G1 phase, while decreasing the expression of CLDN1, Bcl‐2, C‐myc, and PCNA with suppressed proliferation, migration, and invasion. Collectively, the current study supports the notion that miR‐98 plays an inhibitory role in human CRC cell proliferation, migration, and invasion and act as a contributor for cell apoptosis by downregulating CLDN1. The current study highlights a potential future strategy to help prevent the development of CRC.

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Hsa-miR-875-5p exerts tumor suppressor function through down-regulation of EGFR in colorectal carcinoma (CRC)

Cited by 29 publications

References 47 publications

Long-chain non-coding RNA GACAT1 promotes development and progression of breast cancer by targeting microRNA-875-3p

Long-chain non-coding RNA GACAT1 promotes development and progression of breast cancer by targeting microRNA-875-3p

microRNA-875-5p plays critical role for mesenchymal condensation in epithelial-mesenchymal interaction during tooth development

Overexpression of microRNA‐98 inhibits cell proliferation and promotes cell apoptosis via claudin‐1 in human colorectal carcinoma

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