microRNAs are a class of short non-coding RNAs containing about 19-22 nucleotides that regulate target gene expression through post-transcriptional repression or mRNA degradation, and involved in a variety of biological processes, such as cellular differentiation, proliferation, apoptosis and metabolism. microRNA-182 (miR-182), belonging to miR-183/96/182 cluster that consists of miR-182, -183, and -96, highly expresses in many cells and tissues, including osteoblasts, lymphocytes, adipocytes, retina, inner ear, etc. The recent studies of miR-182 highlighted its multiple important roles in differentiation, development, and functional maintenance in the cells and tissues. The dysregulation of miR-182 is associated with occurrence and development of many diseases, such as retinopathy, autoimmune diseases, cancers, obesity and diabetes. This review summarizes recent research progresses on the roles and mechanisms of miR-182 in cellular function and diseases.
Apoptosis ; Cell Differentiation ; MicroRNAs ; genetics ; Neoplasms ; Osteoblasts

OBJECTIVE: To investigate the regulatory effect of miRNA-29a-3p (miR-29a-3p ) on hepatoma-derived growth factor (HDGF), and its influences on the proliferation and apoptosis of acute lymphoblastic leukemia (ALL) cell line E6-1. METHODS: Thirty-five patients with ALL treated in our hospital from January 2017 to January 2019 were selected as research objects, and 35 adults who underwent physical examination in the same period were selected as healthy control group. The miR-29a-3p overexpression vector, miR-29a-3p inhibitory expression vector, and miR-29a-3p and HDGF co-overexpression vector were transfected into E6-1 cells. The expression levels of miR-29a-3p and HDGF mRNA were detected by RT-qPCR. The expression of protein was detected by Western blot. The targeting relationship between miR-29a-3p and HDGF was detected by dual luciferase reporter assay. The cell proliferation was detected by CCK-8 method, while apoptosis detected by flow cytometry. RESULTS: Compared with healthy control group, HDGF was highly expressed in serum of patients with ALL and leukemia cells HuT 78, E6-1, CCRF-CEM, while miR-29a-3p was low expressed (P<0.05). After overexpression of miR-29a-3p , the expression levels of CyclinD1 and Bcl-2 in leukemia cells E6-1 were significantly reduced, while the expression levels of p21 and Bax were significantly increased (P<0.05). The activity of E6-1 cells was also significantly reduced, while the apoptosis rate of E6-1 cells was significantly increased (P<0.05). miR-29a-3p could target and regulate the expression of HDGF, while overexpression of HDGF reversed the inhibitory effect of miR-29a-3p overexpression on the proliferation and promotion effect on the apoptosis of leukemia cells E6-1. CONCLUSION Overexpression of miR-29a-3p can inhibit the proliferation and promote the apoptosis of ALL cells E6-1, and its mechanism may be related to the regulation of HDGF expression.
Humans ; Apoptosis ; Cell Proliferation ; Leukemia ; MicroRNAs/genetics*

MicroRNAs (miRNAs) are endogenous non-coding single-stranded small RNAs that regulate gene expression by recognizing homologous sequences and interfering with transcriptional, translational or epigenetic processes. MiRNAs are involved in a variety of disease processes, and regulate the physiological and pathological status of diseases by modulating target cell activity, migration, invasion, apoptosis, autophagy and other processes. Among them, let-7i is highly expressed in various systems, which participates in the process of tumors, cardiovascular and cerebrovascular diseases, fibrotic diseases, inflammatory diseases, neurodegenerative diseases and other diseases, and plays a positive or negative regulatory role in these diseases through different signal pathways and key molecules. Moreover, it can be used as an early diagnosis and prognostic marker for a variety of diseases and become a potential therapeutic target. As a biomarker, let-7i is frequently tested in combination with other miRNAs to diagnose multiple diseases and evaluate the clinical treatment or prognosis.
Biomarkers ; Apoptosis ; Autophagy ; Epigenesis, Genetic ; MicroRNAs/genetics*

OBJECTIVE: To study the role of microRNA-17-5p (miR-17-5p) in the pathogenesis of pediatric nephrotic syndrome (NS) and its effect on renal podocyte apoptosis via the activin A (ActA)/Smads pathway. METHODS: An analysis was performed on 55 children with NS (NS group) who were admitted from March 2018 to March 2019. Fifty healthy children who underwent physical examination during the same period of time were enrolled as the control group. The mRNA expression of miR-17-5p in peripheral blood was measured and compared between the two groups. Human renal podocytes were transfected with antisense oligonucleotide recombinant plasmid containing miR-17-5p (inhibition group) or control vector containing nonsense random sequence (negative control group), and untreated human renal podocytes were used as the blank group. These groups were compared in terms of cell apoptosis and the mRNA and protein expression of miR-17-5p, ActA, and Smads after transfection. RESULTS: The NS group had a significantly higher level of miR-17-5p in peripheral blood than the control group (P<0.001). Compared with the blank and negative control groups, the inhibition group had significantly lower apoptosis rate and relative mRNA expression of miR-17-5p and significantly higher relative mRNA and protein expression of ActA, Smad2, and Smad3 (P<0.001). CONCLUSIONS There is an increase in the content of miR-17-5p in peripheral blood in children with NS. Low expression of miR-17-5p can inhibit the apoptosis of human renal podocytes, which may be associated with the upregulation of the mRNA and protein expression of ActA, Smad2 and Smad3.
Apoptosis ; Child ; Humans ; MicroRNAs ; genetics ; Nephrotic Syndrome ; genetics ; Podocytes ; Transfection

SIRT3, SIRT4 and SIRT5 are located in mitochondria and also known as mitochondrial sirtuins. They play important roles in regulating many cellular functions including cell survival, cell cycle or apoptosis, DNA repair and metabolism. Mitochondrial sirtuins are involved in the protection of mitochondrial integrity and energy metabolism under stress regulating the expression of neurotransmitter receptors, neurotrophins, extracellular matrix proteins and various transcription factors, thus involved in epileptogenesis triggered by both genetic or acquired factors. Here we review research progress on the actions of mitochondrial sirtuin in epilepsy; and discuss the challenges and perspectives of mitochondrial sirtuin as a potential therapeutic target for epilepsy.
Apoptosis ; Epilepsy/genetics* ; Humans ; Mitochondria/genetics* ; Sirtuin 3 ; Sirtuins

Sp1 is a ubiquitous nuclear factor that plays a key role in maintaining basal transcription of 'house-keeping' genes. It has been demonstrated that Sp1 is involved in many cellular process, e.g.cell growth and differentiation. Sp1 plays an extremely important role in growth and metastasis of many tumors by regulating oncogenes, tumor suppressor genes, cell cycle control molecules, growth-related signal transductions, angiogenesis-related factors, as well as apoptosis. The expression of Sp1 and its activity are strictly regulated. Mechanisms include the modulation of Sp1 and interactions between Sp1 and other molecules. New treatment with Sp1 as the target will bring profound impacts on the strategy of clinical chemotherapy of tumor.
Apoptosis ; genetics ; Humans ; Neoplasm Metastasis ; genetics ; Neoplasms ; genetics ; Sp1 Transcription Factor ; genetics ; metabolism

To explore the expression spectra of apoptosis-related gene pnas-2 in normal tissues and acute leukemia (AL) patient tissues, the expressions of pnas-2 gene in tissues including heart, brain, placenta, lung, liver, skeletal muscle, kidney, pancreas, spleen, lymph node, thymus, leukocyte, bone marrow and fetal liver were detected by Northern blot. The expressions of pnas-2 in samples including 44 de novo, 9 non-CR, 27 CR and 12 relapsed AL patients were measured by real-time RT-PCR and Northern blot, and the expression levels of pnas-2 in normal and tumor tissues from 31 patients with malignancies were also detected. The results showed that pnas-2 was not expressed in the most tissues except in placenta. The results of real-time PCR indicated that pnas-2 expressions in samples of de novo, non-CR and relapsed patients ware significantly higher than that in CR, tumor tissues and normal tissues. In serial monitoring of 7 AL patients, the expression level of pnas-2 was high at first visit examination, but remarkably decreased after remission, and the pnas-2 expression level increased again when relapsed. It is concluded that the pnas-2 is specifically up-regulated in acute leukemia patients, which might be an oncogene and participate in leukemogenesis.
Acute Disease ; Apoptosis ; genetics ; Apoptosis Regulatory Proteins ; genetics ; metabolism ; Biomarkers, Tumor ; genetics ; Gene Expression Regulation, Leukemic ; Humans ; Leukemia ; pathology

Animals ; Apoptosis ; genetics ; immunology ; Apoptosis Regulatory Proteins ; genetics ; Autoimmune Lymphoproliferative Syndrome ; genetics ; immunology ; physiopathology ; Humans ; Mutation ; T-Lymphocytes ; immunology

OBJECTIVE: To study the expression of BIRC6 in renal cancer tissues and investigate the effect of BIRC6 silencing on apoptosis and autophagy of 786-O cells. METHODS: Twenty surgical specimens of renal cancer tissues and adjacent renal tissues were collected from Meizhou People's Hospital between February, 2016 and December, 2018 for detection of BIRC6 protein expression using immunohistochemistry. Renal cancer 786-O cells were transfected with a control small interfering RNA (siRNA) or BIRC6 siRNA RESULTS: The expression of BIRC6 protein was significantly higher in renal cancer tissues than in the adjacent renal tissues. Western blotting showed that siRNA-mediated silencing of BIRC6 significantly lowered the expression of BIRC6 in 786-O cells. In the cells with BIRC6 silencing, treatment with 12.5, 25, 50, 100 and 200 μg/mL 5-FU resulted in significantly higher proliferation inhibition rates than in the cells transfected with the control siRNA ( CONCLUSIONS Interference of BIRC6 mediated by siRNA can inhibit autophagy and promote 5-FU-induced apoptosis to enhance the sensitivity of 786-O cells to 5-FU.
Apoptosis ; Autophagy ; Cell Line, Tumor ; Cell Proliferation ; Humans ; Inhibitor of Apoptosis Proteins/genetics* ; Kidney Neoplasms/genetics* ; RNA, Small Interfering/genetics*

OBJECTIVETo investigate the effect of siRNA targeting Livin and Survivin gene simultaneously on the proliferation and apoptosis of human colon cancer cells.

METHODSSiRNA recombinant expression vectors targeting Livin and Survivin gene simultaneously were constructed and transfected into human colon cancer cell line Lovo. The effects of siRNA recombinant expression vector on Lovo cells were detected by RT-PCR, Western blot, MTT reduction assay and flow cytometry.

RESULTSIt was confirmed by restriction endonuclease and sequence analysis that siRNA recombinant expression vector targeting Livin and Survivin gene simultaneously was constructed successfully. The suppressive rates of siRNA targeting Livin and Survivin gene simultaneously on Livin mRNA and protein expression were 27.9% and 22.3% respectively, and those on Survivin mRNA and protein expression were 32.2% and 40.9% respectively. The survival rate of cancer cells was decreased whereas the apoptotic rate was increased, but the coordinate repression was weaker than Livin and Survivin RNA interference alone.

CONCLUSIONSsiRNA targeting Livin and Survivin gene simultaneously can decrease the expression of Livin and Survivin gene, suppress cell proliferation and induce cell apoptosis in human colon cancer. The coordinate repression was weaker than Livin and Survivin RNA interference alone.

Adaptor Proteins, Signal Transducing ; genetics ; Apoptosis ; Cell Line, Tumor ; Colonic Neoplasms ; genetics ; pathology ; Humans ; Inhibitor of Apoptosis Proteins ; genetics ; Microtubule-Associated Proteins ; genetics ; Neoplasm Proteins ; genetics ; RNA, Small Interfering