FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4283658051> ?p ?o ?g. }

• W4283658051 endingPage "13" @default.
• W4283658051 startingPage "1" @default.
• W4283658051 abstract "Colorectal cancer (CRC) is the third most diagnosed cancer worldwide and the second leading cause of cancer-related deaths. Many researchers have reported that abnormal microRNAs (miRs) were expressed in CRC and participated in the occurrence and progression of CRC. However, there are few reports of miR-887-3p regulating CRC development. In the current study, we investigated the abnormal expression of miR-887-3p and also demonstrated its regulatory role and detailed molecular mechanism in CRC. Initially, miRNA expression data were obtained from TCGA-COAD that consisted of 453 CRC samples and 8 normal tissue samples. These were downloaded and analyzed to compare the expression level of miR-887-3p in CRC tissues to that in normal tissues. Moreover, 32 pairs of surgically resected CRC tumors and para-cancer tissues from our hospital were collected. Quantitative real-time PCR (qRT-PCR) was performed to detect miR-887-3p expression levels in CRC tissues, para-cancer tissues, several CRC cell lines, and an intestinal epithelial cell line. Following miR-887-3p mimic transfection in colon cancer SW480 cell line, the regulatory roles of miR-887-3p on cell proliferation, apoptosis, invasion, migration, and epithelial-mesenchymal transition (EMT) were detected through CCK-8, flow cytometry, transwell assay, and Western blot. After potential targeting protein was predicted by bioinformatic websites, the luciferase reporter assay and Western blot were used to confirm the target of miR-887-3p. The targeting protein expressions were detected by Western blot and qRT-PCR. The relationship between miR-887-3p level and the effect of miR-887-3p on P53 expression was evaluated by Western blot and qRT-PCR. The effects of miR-887-3p on CRC cell growth in vivo by xenograft tumor experiments were investigated, and Ki-67 in tumor tissue was determined by immunohistochemistry. Results. The COAD data demonstrated that the expression levels of miR-887-3p in CRC clinical sample tissues and cell line cultures were remarkably lower than para-cancer normal tissues and NCM460 cells (normal colonic epithelial cell line). Functional experiments demonstrated that overexpression of miR-887-3p in SW480 cells significantly reduced proliferation, migration, invasion, and EMT, and promoted cancer cell apoptosis. Additionally, Western blot, qRT-PCR, and luciferase reporter assays confirmed that DNMT1 was a downstream target of miR-887-3p. Moreover, the blocking of DNMT1 by miR-887-3p mimics also promoted P53 expression. Finally, overexpression of DNMT1 in SW480 cells could partially reverse the regulatory effect of miR-887-3p mimics on CRC cell development. From in vivo experiments, overexpression of miR-887-3p could inhibit tumor growth in CRC xenograft mice and reduce the Ki-67 level. Conclusion. The microRNA miR-887-3p is a potential biomarker of CRC. It inhibited CRC cell proliferation, invasion, and EMT, and promoted cell apoptosis through targeting and downregulating DNMT1 and promoting P53 expression. Therefore, miR-887-3p may be a good biomarker and therapeutic target for CRC treatment." @default.
• W4283658051 created "2022-06-29" @default.
• W4283658051 creator A5002072084 @default.
• W4283658051 creator A5014010282 @default.
• W4283658051 creator A5031246081 @default.
• W4283658051 creator A5052582632 @default.
• W4283658051 creator A5072746457 @default.
• W4283658051 creator A5079948316 @default.
• W4283658051 creator A5084068598 @default.
• W4283658051 date "2022-06-27" @default.
• W4283658051 modified "2023-10-13" @default.
• W4283658051 title "miR-887-3p Inhibits the Progression of Colorectal Cancer via Downregulating DNMT1 Expression and Regulating P53 Expression" @default.
• W4283658051 cites W1529595331 @default.
• W4283658051 cites W1959021249 @default.
• W4283658051 cites W1976612131 @default.
• W4283658051 cites W1986639355 @default.
• W4283658051 cites W1989421786 @default.
• W4283658051 cites W2020394652 @default.
• W4283658051 cites W2059876640 @default.
• W4283658051 cites W2075214050 @default.
• W4283658051 cites W2097126123 @default.
• W4283658051 cites W2115761146 @default.
• W4283658051 cites W2132005991 @default.
• W4283658051 cites W2162674813 @default.
• W4283658051 cites W2166632917 @default.
• W4283658051 cites W2168241534 @default.
• W4283658051 cites W2193151864 @default.
• W4283658051 cites W2204245753 @default.
• W4283658051 cites W2346753238 @default.
• W4283658051 cites W2412814044 @default.
• W4283658051 cites W2521535110 @default.
• W4283658051 cites W2529803091 @default.
• W4283658051 cites W2605200743 @default.
• W4283658051 cites W2618842626 @default.
• W4283658051 cites W2741541139 @default.
• W4283658051 cites W2745763239 @default.
• W4283658051 cites W2751893550 @default.
• W4283658051 cites W2770097243 @default.
• W4283658051 cites W2772342845 @default.
• W4283658051 cites W2794857100 @default.
• W4283658051 cites W2884218599 @default.
• W4283658051 cites W2889646458 @default.
• W4283658051 cites W2899349638 @default.
• W4283658051 cites W2955537519 @default.
• W4283658051 cites W2979406301 @default.
• W4283658051 cites W2995553248 @default.
• W4283658051 cites W3024231418 @default.
• W4283658051 cites W3033369742 @default.
• W4283658051 cites W3044776979 @default.
• W4283658051 cites W3081618078 @default.
• W4283658051 cites W3085820762 @default.
• W4283658051 cites W3088598065 @default.
• W4283658051 cites W3113245087 @default.
• W4283658051 cites W3128544040 @default.
• W4283658051 cites W3128646645 @default.
• W4283658051 cites W3158158224 @default.
• W4283658051 cites W3158740926 @default.
• W4283658051 cites W3209630987 @default.
• W4283658051 cites W393883301 @default.
• W4283658051 cites W4207076067 @default.
• W4283658051 doi "https://doi.org/10.1155/2022/7179733" @default.
• W4283658051 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35795731" @default.
• W4283658051 hasPublicationYear "2022" @default.
• W4283658051 type Work @default.
• W4283658051 citedByCount "20" @default.
• W4283658051 countsByYear W42836580512022 @default.
• W4283658051 countsByYear W42836580512023 @default.
• W4283658051 crossrefType "journal-article" @default.
• W4283658051 hasAuthorship W4283658051A5002072084 @default.
• W4283658051 hasAuthorship W4283658051A5014010282 @default.
• W4283658051 hasAuthorship W4283658051A5031246081 @default.
• W4283658051 hasAuthorship W4283658051A5052582632 @default.
• W4283658051 hasAuthorship W4283658051A5072746457 @default.
• W4283658051 hasAuthorship W4283658051A5079948316 @default.
• W4283658051 hasAuthorship W4283658051A5084068598 @default.
• W4283658051 hasBestOaLocation W42836580511 @default.
• W4283658051 hasConcept C104317684 @default.
• W4283658051 hasConcept C121608353 @default.
• W4283658051 hasConcept C145059251 @default.
• W4283658051 hasConcept C153911025 @default.
• W4283658051 hasConcept C190283241 @default.
• W4283658051 hasConcept C2776415932 @default.
• W4283658051 hasConcept C2779013556 @default.
• W4283658051 hasConcept C48023723 @default.
• W4283658051 hasConcept C502942594 @default.
• W4283658051 hasConcept C526805850 @default.
• W4283658051 hasConcept C54009773 @default.
• W4283658051 hasConcept C54355233 @default.
• W4283658051 hasConcept C553184892 @default.
• W4283658051 hasConcept C62112901 @default.
• W4283658051 hasConcept C76419328 @default.
• W4283658051 hasConcept C81885089 @default.
• W4283658051 hasConcept C86803240 @default.
• W4283658051 hasConceptScore W4283658051C104317684 @default.
• W4283658051 hasConceptScore W4283658051C121608353 @default.
• W4283658051 hasConceptScore W4283658051C145059251 @default.
• W4283658051 hasConceptScore W4283658051C153911025 @default.
• W4283658051 hasConceptScore W4283658051C190283241 @default.

• next