دورية أكاديمية

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

التفاصيل البيبلوغرافية
العنوان: Overexpression of microRNA-98 inhibits cell proliferation and promotes cell apoptosis via claudin-1 in human colorectal carcinoma.
المؤلفون: Zheng YF; Department of Gastrointestinal Surgery, The First Affiliated Hospital of Shantou University Medical College, Shantou, China., Luo J; Department of Hepatobiliary Surgery, The First Affiliated Hospital of Shantou University Medical College, Shantou, China., Gan GL; Department of Gastrointestinal Surgery, The First Affiliated Hospital of Shantou University Medical College, Shantou, China., Li W; Department of Gastrointestinal Surgery, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.
المصدر: Journal of cellular biochemistry [J Cell Biochem] 2019 Apr; Vol. 120 (4), pp. 6090-6105. Date of Electronic Publication: 2018 Dec 02.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Wiley-Liss Country of Publication: United States NLM ID: 8205768 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1097-4644 (Electronic) Linking ISSN: 07302312 NLM ISO Abbreviation: J Cell Biochem Subsets: MEDLINE
أسماء مطبوعة: Publication: <2004>- : Hoboken, NJ : Wiley-Liss
Original Publication: New York : Liss, c1982-
مواضيع طبية MeSH: Apoptosis/*genetics , Cell Proliferation/*genetics , Claudin-1/*metabolism , Colorectal Neoplasms/*metabolism , MicroRNAs/*metabolism, Cell Movement/genetics ; Claudin-1/genetics ; Colorectal Neoplasms/pathology ; Female ; Gene Expression Regulation, Neoplastic/genetics ; HCT116 Cells ; HT29 Cells ; Humans ; Male ; MicroRNAs/genetics ; Middle Aged ; Neoplasm Invasiveness/genetics ; Transcriptome ; Transfection
مستخلص: 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.
(© 2018 Wiley Periodicals, Inc.)
فهرسة مساهمة: Keywords: apoptosis; claudin-1 (CLDN1); colorectal carcinoma (CRC); invasion; microRNA-98 (miR-98); migration; proliferation
المشرفين على المادة: 0 (CLDN1 protein, human)
0 (Claudin-1)
0 (MIRN98 microRNA, human)
0 (MicroRNAs)
تواريخ الأحداث: Date Created: 20181204 Date Completed: 20200721 Latest Revision: 20200721
رمز التحديث: 20231215
DOI: 10.1002/jcb.27895
PMID: 30506722
قاعدة البيانات: MEDLINE
الوصف
تدمد:1097-4644
DOI:10.1002/jcb.27895