ABSTRACT
OBJECTIVE: To investigate the effect of lncRNA-CASC2 (CASC2) /miR-155-5p/APC axis to the progression of non-Hodgikn lymphoma (NHL). METHODS: The expression level of CASC2 and miR-155-5p in NHL cell lines were examined by qRT-PCR. Dual-luciferase reporter gene assay was used to verify the relationship between miR-155-5p, CASC2 and APC. The effects of CASC/miR-155-5p/APC axis to the proliferation, invasion and apoptosis of NK-92 cells were detected by MTT, Transwell assay and flow cytometry assay, respectively. RESULTS: CASC2 was downregulated in NHL cell lines. Overexpression of CASC2 could inhibit the proliferation and invasion of NK-92 cells, and promote its apoptosis. Dual-luciferase reporter gene assay confirmed that there was a targeting relationship between miR-155-5p, CASC2 and APC. The restoration experiments proved that knockdown of both miR-155-5p and CASC2 or APC could restore the inhibitory effect of miR-155-5p silencing to the biological behavior of NK-92 cells. CONCLUSION: Overexpression of CASC2 suppresses the proliferation and invasion of NK-92 cells, promote the apoptosis of NK-92 cells via targeting miR-155-5p and upregulating APC expression.
Subject(s)
Lymphoma, Non-Hodgkin , MicroRNAs , RNA, Long Noncoding , Cell Line, Tumor , Gene Expression Regulation, Neoplastic , Humans , Lymphoma, Non-Hodgkin/genetics , MicroRNAs/genetics , RNA, Long Noncoding/genetics , Tumor Suppressor Proteins/geneticsABSTRACT
PURPOSE: The work outlined herein investigated the prognosis value and the potential role son of sevenless homolog 1 (SOS1) played in uveal melanoma (UM). METHODS: We analyzed the mRNA expression level of SOS1 in primary UM cells based on the GSE44295 dataset obtained from the Gene Expression Omnibus (GEO, http://www.ncbi.nlm.nih.gov/geo/ ) database. The correlation between SOS1 expression and clinical characteristics were analyzed by Chi-squared (χ2) test. Then we used SOS1 siRNA to downregulate SOS1 expression in M23 cells. The effect of knockdown SOS1 on cell proliferation was studied using the Cell-Counting Kit-8 and colony formation assays. The influence of silencing SOS1 on cell motility was explored using wound-healing assays and transwell assays. In addition, the relationship between SOS1 and the MAPK signaling pathway was analyzed by western blot. RESULTS: Our results demonstrated that the mRNA expression level of SOS1 was markedly upregulated in UM cells (p < 0.001) and correlated with poor prognosis in UM patients (p = 0.015). Moreover, SOS1 mRNA expression level was found to be positively associated with histological-type (p = 0.043) and death (p = 0.012). Knockdown of SOS1 caused an inhibition on M23 cell proliferation, migration, and invasion. Moreover, the phosphorylation levels of MEK and ERK were reduced in UM cells after downregulating SOS1 expression (p < 0.010). CONCLUSION: Our data demonstrated that SOS1 might play a facilitating role in M23 cell growth and motility by regulating the MAPK signaling pathway. Furthermore, the data suggested that SOS1 may serve as an UM predictor of prognosis as well as a therapeutic target.
Subject(s)
Biomarkers, Tumor/metabolism , Gene Expression Regulation, Neoplastic , Melanoma/pathology , SOS1 Protein/metabolism , Uveal Neoplasms/pathology , Biomarkers, Tumor/genetics , Case-Control Studies , Cell Movement , Cell Proliferation , Female , Follow-Up Studies , Humans , Male , Melanoma/genetics , Melanoma/metabolism , Middle Aged , Prognosis , RNA, Small Interfering/genetics , SOS1 Protein/antagonists & inhibitors , SOS1 Protein/genetics , Survival Rate , Tumor Cells, Cultured , Uveal Neoplasms/genetics , Uveal Neoplasms/metabolismABSTRACT
In this paper, effect and molecular mechanism of sika pilose antler type I collagen(SPC-I) of ROS1728 cell were explored. For the SPC-I provides the theory basis for the treatment of osteoporosis. The adherent method was used to cultivate rat osteosarcoma osteogenesis sample cell line ROS1728. The effect of SPC-I on ROS1728 cells proliferation was tested by CCK-8 method. Runx2, osernix, ALP, Coll-I, OC osteogenesis related genes expression was tested by RT-PCR, and Runx2 protein expression was tested by Western-bolt. Results showed that 5 gâ¢L ⻹ SPC-I could inhibit ROS1728 cell proliferation, and significantly promote the expression of ROS1728 cell specific transcription factor Runx2 and osterix mRNA, Runx2 protein and marker gene ALP, Coll-I, OC mRNA expression(P<0.01). 2.5 gâ¢L ⻹ and 10 gâ¢L ⻹ SPC-I could significantly inhibit the ROS1728 cell proliferation(P<0.01), and inhibit the expression of related genes. In conclusion, 5 gâ¢L ⻹ SPC-I could inhibit ROS1728 cell proliferation, obviously enhance ROS1728 cell function, promote ROS1728 cell differentiation, maturation.
Subject(s)
Antlers/chemistry , Collagen/pharmacology , Osteoblasts/drug effects , Osteogenesis , Animals , Cell Differentiation , Cell Line, Tumor , Cell Proliferation , RatsABSTRACT
In the crystal structure of the title compound, C(8)H(10)N(2)O(3), mol-ecules are linked by N-Hâ¯O hydrogen bonds, forming ribbons of centrosymmetric dimers extending along the c axis.
