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1.
J Orthop Surg Res ; 17(1): 332, 2022 Jun 27.
Article in English | MEDLINE | ID: mdl-35761386

ABSTRACT

BACKGROUND: As a skeletal malignancy, osteosarcoma has high incidence among primary malignant bone tumors. With increasing researches on molecules which mediate cancer progression, molecular mechanism has gradually become the pivot of osteosarcoma research and treatment. AIM: Our study aimed at investigating the function of G3BP stress granule assembly factor 2 (G3BP2), which is an oncogene for breast cancer (BC) and prostate cancer but remains unknown in osteosarcoma cells. METHODS: Related gene expression was confirmed by RT-qPCR. Functional assays including immunofluorescence (IF), colony formation, transferase-mediated dUTP nick-end labeling (TUNEL) as well as transwell assays were utilized to test the cell biological process caused by the genes. Meanwhile, RNA pull-down assay, along with luciferase reporter and RNA immunoprecipitation (RIP) assays, was utilized to detect the interaction G3BP2, miR-124-3p and FGD5 antisense RNA 1 (FGD5-AS1) may exert on the regulation of osteosarcoma cells. RESULTS: G3BP2 was with high expression in osteosarcoma cells, and it aggravated the malignant cell behaviors in osteosarcoma. Additionally, miR-124-3p was verified to negatively regulate G3BP2 expression in osteosarcoma cells. Moreover, lncRNA FGD5-AS1 was predicted and testified to be the sponge of miR-124-3p and modulated G3BP2 expression positively. Subsequently, FGA5-AS1 accelerated osteosarcoma cell proliferation through up-regulating G3BP2. Furthermore, we identified EBF transcription factor 1 (EBF1) as the transcription factor for FGA5-AS1, and EBF1 served as a tumor facilitator in osteosarcoma cells. CONCLUSION: EBF1 induced-FGA5-AS1 aggravated osteosarcoma cell malignancy by targeting miR-124-3p and G3BP2.


Subject(s)
Bone Neoplasms , MicroRNAs , Osteosarcoma , RNA, Long Noncoding , RNA-Binding Proteins , Trans-Activators , Adaptor Proteins, Signal Transducing/genetics , Adaptor Proteins, Signal Transducing/metabolism , Apoptosis/genetics , Bone Neoplasms/genetics , Cell Line, Tumor , Cell Movement/genetics , Cell Proliferation/genetics , Gene Expression Regulation, Neoplastic , Guanine Nucleotide Exchange Factors/genetics , Guanine Nucleotide Exchange Factors/metabolism , Humans , MicroRNAs/genetics , MicroRNAs/metabolism , Osteosarcoma/genetics , Osteosarcoma/pathology , RNA, Long Noncoding/genetics , RNA, Long Noncoding/metabolism , RNA-Binding Proteins/genetics , RNA-Binding Proteins/metabolism , Trans-Activators/genetics , Trans-Activators/metabolism , Transcription Factors/genetics , Up-Regulation/genetics
2.
Article in English | WPRIM (Western Pacific) | ID: wpr-928983

ABSTRACT

Brain-lung-thyroid syndrome is a rare autosomal dominant disorder. More than 100 cases have been reported worldwide, but few cases have been reported in China. In December 2018, a boy with brain-lung-thyroid syndrome, aged 3 years and 10 months, was admitted to Xiangya Hospital of Central South University due to repeated cough for more than 3 years. In infancy of the boy, psychomotor retardation, repeated cough, and hypothyroidism were found. Gene detection showed that there was c.927delc heterozygous variation in NKX2-1 gene (NM-001079668: exon3: c.927delC). The variation of this gene locus has not been reported in relevant literature so far, which indicates a new mutation. According to the above clinical manifestations and examination results, the boy was diagnosed as brain-lung-thyroid syndrome, which mainly characterized by nervous system disorders, accompanied by respiratory manifestations and hypothyroidism. The boy was treated with oral dopasehydrazine to relieve tremor and levothyroxine sodium tablets to relieve hypothyroidism. Anti-infection, atomization, rehabilitation training and other symptomatic supporting treatment were also administered. The boy's language and movement have improved, the thyroid hormone level is normal, and there are still repeated respiratory tract infections.


Subject(s)
Humans , Male , Athetosis/genetics , Chorea , Congenital Hypothyroidism/genetics , Cough , Respiratory Distress Syndrome, Newborn , Thyroid Nuclear Factor 1/genetics
3.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-828691

ABSTRACT

A girl, aged 12 years, was admitted due to fever and rash for 3 days. The child developed recurrent high fever and rash on both lower extremities 3 days before, and the rash on left lower extremity quickly merged into a patch within 24 hours, with hemorrhage and necrosis in black and purple, large vesicles, and blisters in the center. Laboratory examination showed a reduction in platelet count and significant increases in fibrinogen and D-dimer during the course of the disease. The child was diagnosed with purpura flulminans. She was given meropenem combined with linezolid for anti-infection, injection of gamma globulin for immunoregulation, and low-molecular-weight heparin for anticoagulation. The fluid in the rash blisters was drawn and the wound was treated to prevent infection. The child's temperature returned to normal, with improvement in gangrene. She was discharged after platelet count, fibrinogen, and D-dimer had returned to normal. Purpura fulminans is a rare thrombotic hemorrhagic disease with rapid progression and is commonly seen in children. Without timely treatment, it may cause severe sequelae with high disability and mortality rates. Anti-infection, correction of coagulation function, and local management of gangrene skin are of great importance during treatment.


Subject(s)
Child , Female , Humans , Blister , Exanthema , Fever , Lower Extremity , Necrosis
4.
Exp Ther Med ; 17(3): 1912-1918, 2019 Mar.
Article in English | MEDLINE | ID: mdl-30783468

ABSTRACT

The aim of the present study was to investigate the effect of microRNA (miR)-34a on spinal cord injury (SCI)-induced inflammation and the possible underlying mechanisms. The results indicated that miR-34a expression was downregulated in a rat model of SCI compared with the control group. Furthermore, miR-34a knockdown was demonstrated to aggravate inflammation, inhibit cell proliferation and enhance apoptosis in an in vitro model of SCI. MiR-34a inhibition was demonstrated to upregulate the expression of inducible nitric oxide synthase and nitric oxide, as well as inducing the expression of toll-like receptor 4 (TLR4) and high mobility group box-1 (HMGB-1) in an in vitro model of SCI. TLR4 inhibitor reduced the effects of miR-34a downregulation on inflammation and cell growth in SCI. Together, these results suggest that miR-34a is able to alleviate SCI via inhibiting HMGB-1 expression in TLR4 signaling.

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