1,752,103 research outputs found
MicroRNA-582-5p promotes triple-negative breast cancer invasion and metastasis by antagonizing CMTM8
No full textTriple-negative breast cancer (TNBC) commonly have aggressive properties. microRNA-582-5p (miR-582-5p) modulates the progression of several cancers. Yet, the role of miR-582-5p in TNBC progression is undetermined. In the current study, we investigated miR-582-5p expression levels and clinical significance in TNBC. The impact of miR-582-5p modulation on the biological behaviors of TNBC cells were measured. The downstream gene(s) regulated by miR-582-5p in TNBC was explored. We showed that compared to adjacent normal breast tissues, the miR-582-5p level was elevated in TNBC samples. The upregulation of miR-582-5p correlated with lymph node metastasis. Overexpression of miR-582-5p enhanced TNBC cell migration and invasion, whereas knockdown of miR-582-5p had an adverse impact on aggressive phenotype. In vivo xenograft mouse studies demonstrated that miR-582-5p overexpression accelerated TNBC growth and metastasis. Mechanistically, miR-582-5p selectively inhibited CMTM8, leading to a reduction of CMTM8 expression. CMTM8 showed suppressive effects on TNBC cell migration and invasion. Rescue experiments revealed that overexpression of CMTM8 impaired miR-582-5p-induced migration and invasion in TNBC cells. Overall, our data uncover an oncogenic role for miR-582-5p in TNBC metastasis through inhibition of CMTM8. We suggest miR-582-5p as a promising target for managing TNBC.</p
MicroRNA-582-3p regulates osteoporosis through regulating homeobox A10 and osteoblast differentiation
No full textRecent studies have demonstrated that micro RNAs (miRNAs) are involved in bone formation and bone cell differentiation, but the role of miR-582-3p in osteoporosis is unclear. We want to study the mechanism of miR-582-3p on osteogenic differentiation. The expression of miR-582-3p and homeobox (Hox) A10 were analyzed by quantitative RT-PCR. The expression levels of HOXA10 protein were determined by Western blot. The target of HOXA10 was identified by bioinformatics and luciferase reporter gene assay. The results showed that miR-582-3p was up-regulated in OP tissues and down-regulated in osteogenic differentiated C2C12 cells compared with that in the control group. Overexpression of miR-582-3p resulted in reduced expression levels of osteocalcin (OC), alkaline phosphatase (ALP), and collagen, type I, α1 (COL1A1). miR-582-3p had a potential binding site with HOXA10. Moreover, miR-582-3p inhibited the expression of HOXA10, and overexpression of HOXA10 reduced the effect of miR-582-3p on osteoblast markers. HOXA10 was the target gene of miR-582-3p, which could inhibit the expression of HOXA10. Furthermore, HOXA10 reduced the role of miR-582-3p in osteoblast markers. miR-582-3p inhibited the development of osteoporosis by regulating HOXA10 and osteoblast differentiation. miR-582-3p may be a therapeutic target of osteoporosis treatment.</p
Participant 582 Community Conversations Interview
No full textIn this interview, Participant 582 shares their experience contracting COVID-19 and suffering from long COVID despite following all the guidelines. The participant says their entire family had COVID-19 and all of them had differing symptoms. The participant expresses their wish that there were more direct and consistent guidelines related to COVID-19 from the officials.New Jersey Department of Healt
Additional file 1: Figure S1. of miR-582-5P induces colorectal cancer cell proliferation by targeting adenomatous polyposis coli
No full textReal-time PCR (left) and western blotting analysis (right) of APC expression in COLO205 cells transfected with miR-582-5P or miR-582-5P-in as compared to NC cells. (TIF 109 kb
MiR-582-5p directly binds to NOTH1 3’UTR in NCI-H358 cell.
No full text(A) Illustration showed the predicted binding site between miR-582-5p and WT-3'UTR-NOTCH1 or Mut-3'UTR- NOTCH1. (B) Dual luciferase reporter assay was conducted to verify the presumptive binding sites. (C) The mRNA level of NOTCH1 was determined with qPCR assay after NCI-H358 cells were transfected with miR-582-5p mimics. (D) The protein level of NOTCH1, NICD1 and Hes-1 was detected by Western blot assay after NCI-H358 cells were transfected with miR-582-5p mimics. (E) Relative expression of NOTCH1 was quantified with Image J and GraphPad Prism 5.0. Data are expressed as the mean ± SD (n = 3). **PP<0.001 versus the scramble group.</p
MiR-582-5p is down-regulated in NSCLC tissues compared with para-carcinoma tissue.
No full text(A) 30 paired NSCLC tissues and para-carcinoma tissues were collected and the expression level of miR-582-5p in both kinds of tissues was detected by using qPCR assay. (B) The expression of miR-582-5p is markedly lower in NSCLC tissues than that in para-carcinoma tissues. (C) qPCR assay was used to determine miR-582-5p expression in the BEAS-2B immortalized human bronchial epithelial cell line and NSCLC cell lines, including A549, NCI-H23, NCI-H358, NCI-H1975 and PC-9. Data are expressed as mean ± SD. *PPP < 0.001 versus the normal tissues’ group or BEAS-2B group.</p
Data_Sheet_1_MicroRNA-582-5p Contributes to the Maintenance of Neural Stem Cells Through Inhibiting Secretory Protein FAM19A1.pdf
No full textEpigenetic regulations on the maintenance of neural stem cells (NSCs) are complicated and far from been fully understood. Our previous findings have shown that after blocking Notch signaling in NSCs in vivo, the stemness of NSCs decreases, accompanied by the downregulated expression of miR-582-5p. In the current study, we further investigated the function and mechanism of miR-582-5p in the maintenance of NSCs in vitro and in vivo. After transfecting a mimic of miR-582-5p, the formation of neurospheres and proliferation of NSCs and intermediate progenitor cells (NS/PCs) were enhanced, and the expression of stemness markers such as Sox2, Nestin, and Pax6 also increased. The results were reversed after transfection of an inhibitor of miR-582-5p. We further generated miR-582 knock-out (KO) mice to investigate its function in vivo, and we found that the number of NSCs in the subventricular zone (SVZ) region decreased and the number of neuroblasts increased in miR-582 deficient mice, indicating reduced stemness and enhanced neurogenesis of NSCs. Moreover, RNA-sequencing and molecular biological analysis revealed that miR-582-5p regulates the stemness and proliferation of NSCs by inhibiting secretory protein FAM19A1. In summary, our research uncovered a new epigenetic mechanism that regulates the maintenance of NSCs, therefore providing novel targets to amplify NSCs in vitro and to promote neurogenesis in vivo during brain pathology and aging.</p
MicroRNA-582-5p suppresses non-small cell lung cancer cells growth and invasion via downregulating NOTCH1
No full textNon-small cell lung cancer (NSCLC) is the most common cancer worldwide. MicroRNAs have been shown to be correlated with biological processes of various tumors. In this study, we observed that the expression of miR-582-5p was lower in NSCLC tissues than that in para-carcinoma tissues. Ectopic expression of miR-582-5p significantly inhibited NCI-H358 cell proliferation and invasion. Knockdown of miR-582-5p showed the opposite results, with cell growth rate and the invasive capacity of PC-9 cells enhanced. Furthermore, we elucidated that NOTCH1 is a target of miR-582-5p and there is an inverse correlation between miR-582-5p and NOTCH1 expression in NSCLC tissues. Overexpression of NOTCH1 in miR-582-5p-overexpressing NCI-H358 cells could partially reverse the inhibition of cell proliferation and invasion by miR-582-5p. Thus, our research demonstrated that miR-582-5p suppresses NSCLC cell lines’ growth and invasion via targeting oncoprotein NOTCH1 and restoration of miR-582-5p might be feasible therapeutic strategy for NSCLC.</div
Knockdown of miR-582-5p promotes proliferation and invasion of PC-9 cell.
No full text(A) MiR-582-5p inhibitors were transfected into PC-9 cells and the silencing effect was assessed by using qPCR assay. (B) Cell growth rate was measured with CCK-8 assay. (C) The protein level of E-cadherin and Vimentin was detected by Western blot assay after PC-9 cells were transfected with miR-582-5p inhibitors. (D) Relative expression of E-cadherin and Vimentin was analyzed by using Image J software and GraphPad Prism 5.0. (E) The effect on PC-9 cell invasion mediated by miR-582-5p inhibitors was evaluated by Transwell assay. (F) The number of invasive cells was quantified with Image-Pro Plus and GraphPad Prism 5.0. Data are presented as the mean ± SD (n = 3). *PPP<0.001 versus the scramble group.</p
Overexpression of miR-582-5p inhibits proliferation and invasion of NCI-H358 cell.
No full text(A) NCI-H358 cells were transfected with miR-582-5p mimics and then miR-582-5p expression was examined with qPCR assay. (B) After transfection with miR-582-5p mimics, NCI-H358 cell proliferation was measured by using CCK-8 assay at different times (0 h, 24 h, 48 h and 72 h). (C) Western blot assay was performed to determine the expression of E-cadherin and Vimentin. (D) Relative expression of E-cadherin and Vimentin was quantified by using Image J software and GraphPad Prism 5.0. (E) Transwell assay was conducted to evaluate the invasive potential of NCI-H358 cells. (F) Relative invasive cells were estimated with Image-Pro Plus tool and GraphPad Prism 5.0. Data are showed as the mean ± SD (n = 3). *PPP<0.001 versus the scramble group.</p
- …
