Abstract:Slow growth and rapid loss of chondrogenic phenotypes are the major problems affecting chronic cartilage lesions. The role of microRNA-195 (miR-195) and its detailed working mechanism in the fore-mentioned process remains unknown. Fibroblastic growth factor 18 (FGF-18) plays a key role in cartilage homeostasis; whether miR-195 could regulate FGF-18 and its downstream signal pathway in chondrocyte proliferation and maintenance of chondrogenic phenotypes still remains unclear. The present research shows elevated… Show more
“…The procedure was carried out as previously described . HOS and 143B cells after different MALAT1, HDAC4, or miR‐140‐5p intervene were seeded in 96‐well plate and incubated for 48 hours.…”
Section: Methodsmentioning
confidence: 99%
“…The procedure was carried out as previously described. 29 HOS and 143B cells after different MALAT1, HDAC4, or miR-140-5p intervene were seeded in 96-well plate and incubated for 48 hours. The following assays were performed according to the manufacturer's instructions by applying an EDU detection kit (Keygen).…”
Noncoding RNAs regulate the initiation and progression of osteosarcoma (OS). The role of long noncoding RNA metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) playing in OS and whether the function it working out was achieved through HDAC4 pathway remain uncovered. In this study, we illustrated that MALAT1 was upregulated and was correlated with poor prognosis in OS patients. Meanwhile, we demonstrated that a depression of MALAT1 suppressed proliferation and promoted apoptosis in OS cell line HOS and 143B. Further, we verified that MALAT1 exerting its function via upregulating of histone deacetylase 4 (HDAC4). Through an online prediction, a series of luciferase assays and RNA pull‐down assays, we demonstrated that both MALAT1 and HDAC4 were the targets of microRNA‐140‐5p (miR‐140‐5p) via sharing a similar microRNA responding elements. Even further, we revealed that MALAT1 served as a ceRNA of HDAC4 via decoying of miR‐140‐5p. Finally, we proved that MALAT1 promoted OS tumor growth in an in vivo animal study. In summary, the outcomes of this study demonstrated the complex ceRNA network among MALAT, miR‐140‐5p, and HDAC4‐mediated proliferation and apoptosis in OS. This study might provide a new axial in molecular treatment of OS.
“…The procedure was carried out as previously described . HOS and 143B cells after different MALAT1, HDAC4, or miR‐140‐5p intervene were seeded in 96‐well plate and incubated for 48 hours.…”
Section: Methodsmentioning
confidence: 99%
“…The procedure was carried out as previously described. 29 HOS and 143B cells after different MALAT1, HDAC4, or miR-140-5p intervene were seeded in 96-well plate and incubated for 48 hours. The following assays were performed according to the manufacturer's instructions by applying an EDU detection kit (Keygen).…”
Noncoding RNAs regulate the initiation and progression of osteosarcoma (OS). The role of long noncoding RNA metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) playing in OS and whether the function it working out was achieved through HDAC4 pathway remain uncovered. In this study, we illustrated that MALAT1 was upregulated and was correlated with poor prognosis in OS patients. Meanwhile, we demonstrated that a depression of MALAT1 suppressed proliferation and promoted apoptosis in OS cell line HOS and 143B. Further, we verified that MALAT1 exerting its function via upregulating of histone deacetylase 4 (HDAC4). Through an online prediction, a series of luciferase assays and RNA pull‐down assays, we demonstrated that both MALAT1 and HDAC4 were the targets of microRNA‐140‐5p (miR‐140‐5p) via sharing a similar microRNA responding elements. Even further, we revealed that MALAT1 served as a ceRNA of HDAC4 via decoying of miR‐140‐5p. Finally, we proved that MALAT1 promoted OS tumor growth in an in vivo animal study. In summary, the outcomes of this study demonstrated the complex ceRNA network among MALAT, miR‐140‐5p, and HDAC4‐mediated proliferation and apoptosis in OS. This study might provide a new axial in molecular treatment of OS.
“…In human endothelial cells, hsamiR-505 inhibited FGF18 mRNA and protein levels and inhibited the activity of a luciferase reporter containing the 3′UTR of FGF18 (Yang et al 2014) suggesting that this microRNA interacts directly with FGF18 mRNA. Another miRNA that interacts with the 3′UTR of FGF18 is miR-195 (Wang et al 2017). Whether these miRNAs are involved in reproductive physiology or medicine is just being explored, although miR-505 abundance was found to be downregulated in endometrial carcinoma (Chen et al 2016), a tissue in which increased FGF18 mRNA levels have been observed (see section on 'Gynaecological cancers'.…”
Several growth factor families have been shown to be involved in the function of the female reproductive tract. One subfamily of the fibroblast growth factor (FGF) superfamily, namely the FGF8 subfamily (including FGF17 and FGF18), has become important as Fgf8 has been described as an oocyte-derived factor essential for glycolysis in mouse cumulus cells and aberrant expression of FGF18 has been described in ovarian and endometrial cancers. In this review, we describe the pattern of expression of these factors in normal ovaries and uteri in rodents, ruminants and humans, as well as the expression of their receptors and intracellular negative feedback regulators. Expression of these molecules in gynaecological cancers is also reviewed. The role of FGF8 and FGF18 in ovarian and uterine function is described, and potential differences between rodents and ruminants have been highlighted especially with respect to FGF18 signalling within the ovarian follicle. Finally, we identify major questions about the reproductive biology of FGFs that remain to be answered, including (1) the physiological concentrations within the ovary and uterus, (2) which cell types within the endometrial stroma and theca layer express FGFs and (3) which receptors are activated by FGF8 subfamily members in reproductive tissues.Reproduction (2018) 155 R53-R62
“…Immunohistochemical (IHC) staining. The IHC procedure was performed as previously described (31). The LAD tissue specimens were processed as follows: 4% paraformaldehyde fixation, paraffin-embedding, sectioned to 4-µm thickness, deparaffinization, rehydration, hydrogen peroxide incubation, antigen retrieval, blocked in 10% goat serum (Bioworld Technology, Inc., St. Louis Park, MN, USA), primary antibody incubation (anti-HMGA2 and anti-GAPDH) at 4˚C overnight, secondary antibody incubation (goat anti-rabbit IgG H&L; Abcam) at 37˚C for 20 min, streptavidin-horseradish peroxidase complex incubation, diaminobenzidine tetrahydroc hloride (MedChemExpress, Monmouth Junction, NJ, USA) staining, hematoxylin (Amresco, LLC, Solon, OH, USA) and counterstaining.…”
Long non-coding RNAs (lncRNAs) have been reported to be key regulators in various types of cancer, including lung adenocarcinoma (LAD). The roles of the lncRNA differentiation antagonizing non-protein coding RNA (DANCR) and high mobility group AT-hook 2 (HMGA2) in LAD remain unclear. In the present study, it was revealed that the lncRNA DANCR was upregulated in LAD tissue and cell lines, compared with para-tumor tissue and a normal lung cell line. Additionally, elevated DANCR expression was associated with poor prognosis in the patients with LAD. Functionally, the study revealed that knockdown of DANCR inhibited invasion and HMGA2 expression in the LAD cell lines, SPCA1 and A549. Furthermore, HMGA2 was overexpressed in LAD tissue and in SPCA1 and A549 cells, compared with para-tumor tissue and a normal lung cell line. Inhibition of HMGA2 suppressed the invasive ability of SPCA1 and A549 cells, and DANCR promoted the invasive ability via regulation of HMGA2 in SPCA1 and A549 cells. The findings of the present study revealed that DANCR promoted the invasion of LAD cells by positively regulating HMGA2. Thus, a DANCR/HMGA2 axis may be a novel potential target in the molecular treatment of LAD.
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