Background: It was reported that long-noncoding RNAs (lncRNAs) had been identified as a novel class of regulators related to various cancers. RPARP-AS1, a differentially-expressed gene, was found in analysis of the gene expression profile of CRC from GEO database. However, its function has not been clear.
Methods: RPARP-AS1 expression was determined by qPCR and Startbase3 analysis. Knockdown of RPARP-AS1 in CRC cell lines was performed by RNAi technology, named si-RPARP-AS1 HCT116 and si-RPARP-AS1 LoVo. Cell proliferation was examined by CCK8 and colony formation assay. RNA pull-down and Luciferase reporter assay were performed to confirm the interaction between RPARP-AS1 and miR-125a-5p.
Results: In the study, we found that the expression of RPARP-AS1 was significantly up-regulated in CRC tissues and multiple CRC cell lines, which was closely related to poor prognosis of CRC patients. Loss-of-function studies indicated that knockdown of RPARP-AS1 inhibited CRC cell proliferation, migration and invasion in HCT116 and LoVo cell lines. Results of research on the mechanisms showed that RPARP-AS1 functioned as a competitive endogenous RNA (ceRNA) to sponge miR-125a-5p, therefore promoting CRC procession.
Conclusion: In summary, these results indicated that RPARP-AS1/miR-125a-5p axis played a positive role in promoting cell proliferation, migration and invasion in CC. It may be as a biomarker used to evaluate CRC prognosis.
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http://dx.doi.org/10.2147/OTT.S304494 | DOI Listing |
J Vis Exp
January 2025
Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University;
Umbilical cord-derived mesenchymal stromal/stem cells (UC-MSCs) present low immunogenicity and potent immunomodulatory effects for treating various diseases. Human UC-MSCs are a heterogeneous population consisting of three main subpopulations with different cell shapes, proliferation rates, differentiation abilities, and immune regulatory functions. Previously, BAMBIMFGE8 UC-MSCs, the first subgroup successfully isolated from UC-MSCs were found to fail to alleviate lupus nephritis.
View Article and Find Full Text PDFHum Cell
January 2025
Department of Tumor Pathology, Faculty of Medical Sciences, University of Fukui, 23-3 Matsuoka-Shimoaizuki, Eiheiji, Fukui, 910-1193, Japan.
Only a few human ovarian endometrioid carcinoma cell lines are currently available, partly due to the difficulty of establishing cell lines from low-grade cancers. Here, using a cell immortalization strategy consisting of i) inactivation of the p16-pRb pathway by constitutive expression of mutant cyclin-dependent kinase 4 (R24C) (CDK4) and cyclin D1, and ii) acquisition of telomerase reverse transcriptase (TERT) activity, we established a human ovarian endometrioid carcinoma cell line from a 46-year-old Japanese woman. That line, designated JFE-21, has proliferated continuously for over 6 months with a doubling time of ~ 55 h.
View Article and Find Full Text PDFGraefes Arch Clin Exp Ophthalmol
January 2025
National Clinical Research Center for Ocular Diseases, Eye Hospital, Wenzhou Medical University, 270 Xueyuan West Road, Wenzhou, 325027, Zhejiang, China.
Purpose: To investigate whether in diabetic cataract (DC), FoxO1 regulates high glucose (HG)-induced activation of NLRC4/IL-6 inflammatory mediators in human lens epithelial cells (SRA01/04) via the JAK1/STAT1 pathway, leading to cataract formation.
Methods: Expression levels of FoxO1, inflammatory factor IL-6 and inflammatory vesicle NLRC4 were examined in SRA01/04 under high glucose (HG) stress at 25-150 mM. Rat lenses were also cultured using HG medium with or without the addition of the FoxO1 inhibitor AS1842856 and the JAK1 agonist RO8191.
Naunyn Schmiedebergs Arch Pharmacol
January 2025
School of Pharmacy, Jiangxi University of Chinese Medicine, Nanchang, China.
Microglia-mediated neuroinflammation plays a crucial role in Alzheimer's disease (AD). Tinosinenside A (Tis A) is a novel sesquiterpene glycoside isolated from the dried rattan stem of Tinospora sinensis (Lour.) Merr.
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