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RGS16 regulated by let-7c-5p promotes glioma progression by activating PI3K-AKT pathway

《医学前沿（英文）》 2023年 第17卷 第1期   页码 143-155 doi: 10.1007/s11684-022-0929-y

摘要： Gliomas are the most common central nervous system tumours; they are highly aggressive and have a poor prognosis. RGS16 belongs to the regulator of G-protein signalling (RGS) protein family, which plays an important role in promoting various cancers, such as breast cancer, pancreatic cancer, and colorectal cancer. Moreover, previous studies confirmed that let-7c-5p, a well-known microRNA, can act as a tumour suppressor to regulate the progression of various tumours by inhibiting the expression of its target genes. However, whether RGS16 can promote the progression of glioma and whether it is regulated by miR let-7c-5p are still unknown. Here, we confirmed that RGS16 is upregulated in glioma tissues and that high expression of RGS16 is associated with poor survival. Ectopic deletion of RGS16 significantly suppressed glioma cell proliferation and migration both in vitro and in vivo. Moreover, RGS16 was validated as a direct target gene of miR let-7c-5p. The overexpression of miR let-7c-5p obviously downregulated the expression of RGS16, and knocking down miR let-7c-5p had the opposite effect. Thus, we suggest that the suppression of RGS16 by miR let-7c-5p can promote glioma progression and may serve as a potential prognostic biomarker and therapeutic target in glioma.

关键词： RGS16     let-7c-5p     glioma     proliferation     migration    

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Novel variants in LAMA3 and COL7A1 and recurrent variant in KRT5 underlying epidermolysis bullosa in

《医学前沿（英文）》 2022年 第16卷 第5期   页码 808-814 doi: 10.1007/s11684-021-0878-x

摘要： Epidermolysis bullosa (EB) is a group of clinically and genetically heterogeneous diseases characterized by trauma-induced mucocutaneous fragility and blister formation. Here, we investigated five Chinese families with EB, and eight variants including a novel nonsense variant (c.47G>A, p.W16*) in LAMA3, a known recurrent variant (c.74C>T, p.P25L) in KRT5, 2 novel (c.2531T>A, p.V844E; c.6811_6814del, p.R2271fs) and 4 known (c.6187C>T, p.R2063W; c.7097G>A, p.G2366D; c.8569G>T, p.E2857*; c.3625_3635del, p.S1209fs) variants in COL7A1 were detected. Notably, this study identified a nonsense variant in LAMA3 that causes EB within the Chinese population and revealed that this variant resulted in a reduction in LAMA3 mRNA and protein expression levels by nonsense-mediated mRNA decay. Our study expands the mutation spectra of Chinese patients with EB.

关键词： epidermolysis bullosa     LAMA3     COL7A1     KRT5     Chinese families    

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A study on rapid acid chrome black (MB 7) spectrophotometric determination of ClO

Jing DONG, Huilong WANG

《化学科学与工程前沿（英文）》 2011年 第5卷 第2期   页码 245-251 doi: 10.1007/s11705-010-1003-x

摘要： Experiments were conducted to investigate the degradation of 2,6-dinitro- -cresol (DNPC) in the chlorine dioxide (ClO ) catalytic oxidation process. Pure aluminum oxide was used as the catalyst in this process. The degradation of DNPC by ClO using aluminum oxide as catalyst was systematically studied by varying the experimental parameters, such as pH values, catalyst dosage, the initial concentration of DNPC and ClO , reaction time, etc. Under optimal condition (DNPC concentration 39 mg·L , ClO concentration 0.234 g·L , reaction time 15 min, catalyst dosage 4.7 g·L and pH 4.32), almost complete degradation of DNPC can be achieved. The kinetic studies revealed that the ClO catalytic oxidation degradation of DNPC followed pseudo-first-order kinetics with respect to both ClO and DNPC concentration. The repetitive use of the catalyst was investigated along sequential feed-batch trials. The catalyst performed efficiently after five runs. In addition, a simple and convenient method for the determination of ClO in water was developed by using acid chrome black 7 (MB 7) spectrophotometry in this paper.

关键词： chlorine dioxide     2     6-dinitro-p-cresol (DNPC)     aluminum oxide     water treatment     MB 7 spectrophotometry    

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全球首例猪心脏移植人体手术

Sarah C. P. Williams

《工程（英文）》 2022年 第16卷 第9期   页码 6-8 doi: 10.1016/j.eng.2022.07.006

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CRISPR基因编辑作物有望走上消费者的餐桌

Sarah C.P. Williams

《工程（英文）》 2023年 第20卷 第1期   页码 6-8 doi: 10.1016/j.eng.2022.11.002

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地球工程研究从实验室走向现场 News & Highlights

Sarah C.P. Williams

《工程（英文）》 2023年 第27卷 第8期   页码 3-5 doi: 10.1016/j.eng.2023.06.004

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基因组学的发展助力古DNA研究

Sarah C.P. Williams

《工程（英文）》 2023年 第26卷 第7期   页码 9-11 doi: 10.1016/j.eng.2023.05.003

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Non-thermal plasma for exhaust gases treatment

,Marquidia PACHECO P.,Fernando GÓMEZ B.,Joel PACHECO P.,Arturo COLÍN C.,José HUERTAS C.,Hilda FRÍAS P.

《机械工程前沿（英文）》 2015年 第10卷 第3期   页码 301-305 doi: 10.1007/s11465-015-0344-z

摘要：

This article describes a study on a non-thermal plasma device to treat exhaust gases in an internal combustion engine. Several tests using a plasma device to treat exhaust gases are conducted on a Honda GX200-196 cm3 engine at different rotational speeds. A plasma reactor could be efficient in degrading nitrogen oxides and particulate matter. Monoxide and carbon dioxide treatment is minimal. However, achieving 1%–3% degradation may be interesting to reduce the emission of greenhouse gases.

关键词： plasma treatment     NOx     CO     CO2     particulate matter     vehicle    

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Novel mutation c.1210-3C>G in with a poly-T tract of 5T affects mRNA splicing in a Chinese patient

《医学前沿（英文）》 2022年 第16卷 第1期   页码 150-155 doi: 10.1007/s11684-021-0846-5

摘要： Cystic fibrosis (CF) is a rare autosomal recessive disease with only one pathogenic gene cystic fibrosis transmembrane conductance regulator (CFTR). To identify the potential pathogenic mutations in a Chinese patient with CF, we conducted Sanger sequencing on the genomic DNA of the patient and his parents and detected all 27 coding exons of CFTR and their flanking intronic regions. The patient is a compound heterozygote of c.2909G>A, p.Gly970Asp in exon 18 and c.1210-3C>G in cis with a poly-T of 5T (T5) sequence, 3 bp upstream in intron 9. The splicing effect of c.1210-3C>G was verified via minigene assay in vitro, indicating that wild-type plasmid containing c.1210-3C together with T7 sequence produced a normal transcript and partial exon 10-skipping-transcript, whereas mutant plasmid containing c.1210-3G in cis with T5 sequence caused almost all mRNA to skip exon 10. Overall, c.1210-3C>G, the newly identified pathogenic mutation in our patient, in combination with T5 sequence in cis, affects the CFTR gene splicing and produces nearly no normal transcript in vitro. Moreover, this patient carries a p.Gly970Asp mutation, thus confirming the high-frequency of this mutation in Chinese patients with CF.

关键词： cystic fibrosis     CFTR     splicing mutation     minigene    

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巨额资金将助推二氧化碳清除技术走向示范应用

Sarah C.P. Williams

《工程（英文）》 2023年 第22卷 第3期   页码 7-9 doi: 10.1016/j.eng.2023.01.002

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Correlation between serum miR-154-5p and urinary albumin excretion rates in patients with type 2 diabetes

Huiwen Ren, Can Wu, Ying Shao, Shuang Liu, Yang Zhou, Qiuyue Wang

《医学前沿（英文）》 2020年 第14卷 第5期   页码 642-650 doi: 10.1007/s11684-019-0719-3

摘要： This study aimed to investigate the correlation between serum miR-154-5p and urinary albumin to creatinine ratio (UACR) in patients with type 2 diabetes mellitus (T2DM) and the association with biomarkers of inflammation and fibrosis in diabetic kidney disease (DKD). A total of 390 patients with T2DM were divided into three groups: normal albuminuria (UACR<30 mg/g, =136, NA), microalbuminuria (UACR at 30–300 mg/g, =132, MA), and clinical albuminuria (UACR>300 mg/g, =122, CA). Circulating miR-154-5p, inflammatory (C-reactive protein (CRP); erythrocyte sedimentation rate (ESR); and tumor necrosis factor-α (TNF-α) and fibrotic markers (vascular endothelial growth factor (VEGF); transforming growth factor-β1 (TGF-β1); and fibronectin (FN)), and other biochemical indicators were assessed via real-time PCR, enzyme-linked immunosorbent assay, and chemiluminescence assay in patients with T2DM and 138 control subjects (NC). UACR, miR-154-5p, glycated hemoglobin (HbA1c), serum creatinine (sCr), blood urea nitrogen (BUN), ESR, CRP, VEGF, TNF-α, TGF-β1, and FN were significantly higher and the estimated glomerular filtration rate (eGFR) was significantly lower in NA, MA, and CA groups than in NC subjects ( <0.05). Elevated levels of UACR and miR-154-5p were directly correlated with HbA1c, sCr, BUN, ESR, CRP, VEGF, TNF-α, TGF-β1, and FN and negatively correlated with eGFR ( <0.05). miR-154-5p, HbA1c, sCr, BUN, eGFR, ESR, CRP, VEGF, TNF-α, TGF-β1, and FN were important factors affecting UACR. These findings indicated that elevated serum miR-154-5p is significantly correlated with high UACR in patients with T2DM and may offer a novel reference for the early diagnosis of DKD.

关键词： type 2 diabetes mellitus     diabetic kidney disease     miR-154-5p     urinary albumin to creatinine ratio    

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MicroRNA-142-3p and microRNA-142-5p are downregulated in hepatocellular carcinoma and exhibit synergistic

null

《医学前沿（英文）》 2015年 第9卷 第3期   页码 331-343 doi: 10.1007/s11684-015-0409-8

摘要：

MicroRNAs (miRNAs), an important class of small non-coding RNAs, regulate gene expression at the post-transcriptional level. miRNAs are involved in a wide range of biological processes and implicated in different diseases, including cancers. In this study, miRNA profiling and qRT-PCR validation revealed that miR-142-3p and miR-142-5p were significantly downregulated in hepatocellular carcinoma (HCC) and their expression levels decreased as the disease progressed. The ectopic expression of miR-142 significantly reduced HCC cell migration and invasion. Overexpression of either miR-142-3p or miR-142-5p suppressed HCC cell migration, and overexpression of both synergistically inhibited cell migration, which indicated that miR-142-3p and miR-142-5p may cooperatively regulate cell movement. miR-142-3p and miR-142-5p, which are mature miRNAs derived from the 3′- and 5′-strands of the precursor miR-142, target distinct pools of genes because of their different seed sequences. Pathway enrichment analysis showed a strong association of the putative gene targets of miR-142-3p and miR-142-5p with several cell motility-associated pathways, including those regulating actin cytoskeleton, adherens junctions, and focal adhesion. Importantly, a number of the putative gene targets were also significantly upregulated in human HCC cells. Moreover, overexpression of miR-142 significantly abrogated stress fiber formation in HCC cells and led to cell shrinkage. This study shows that mature miR-142 pairs collaboratively regulate different components of distinct signaling cascades and therefore affects the motility of HCC cells.

关键词： hepatocellular carcinoma     microRNA     metastasis     cytoskeletal reorganization    

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抗肥胖症药物市场需求旺盛

Sarah C. P. Williams

《工程（英文）》 2024年 第32卷 第1期   页码 4-6 doi: 10.1016/j.eng.2023.11.005

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lncR-GAS5 upregulates the splicing factor to impair endothelial autophagy, leading to atherogenesis

《医学前沿（英文）》 2023年 第17卷 第2期   页码 317-329 doi: 10.1007/s11684-022-0931-4

摘要： Long noncoding RNAs (lncRNAs) play a critical role in the regulation of atherosclerosis. Here, we investigated the role of the lncRNA growth arrest-specific 5 (lncR-GAS5) in atherogenesis. We found that the enforced expression of lncR-GAS5 contributed to the development of atherosclerosis, which presented as increased plaque size and reduced collagen content. Moreover, impaired autophagy was observed, as shown by a decreased LC3II/LC3I protein ratio and an elevated P62 level in lncR-GAS5-overexpressing human aortic endothelial cells. By contrast, lncR-GAS5 knockdown promoted autophagy. Moreover, serine/arginine-rich splicing factor 10 (SRSF10) knockdown increased the LC3II/LC3I ratio and decreased the P62 level, thus enhancing the formation of autophagic vacuoles, autolysosomes, and autophagosomes. Mechanistically, lncR-GAS5 regulated the downstream splicing factor SRSF10 to impair autophagy in the endothelium, which was reversed by the knockdown of SRSF10. Further results revealed that overexpression of the lncR-GAS5-targeted gene miR-193-5p promoted autophagy and autophagic vacuole accumulation by repressing its direct target gene, SRSF10. Notably, miR-193-5p overexpression decreased plaque size and increased collagen content. Altogether, these findings demonstrate that lncR-GAS5 partially contributes to atherogenesis and plaque instability by impairing endothelial autophagy. In conclusion, lncR-GAS5 overexpression arrested endothelial autophagy through the miR-193-5p/SRSF10 signaling pathway. Thus, miR-193-5p/SRSF10 may serve as a novel treatment target for atherosclerosis.

关键词： lncR-GAS5     miR-193-5p     splicing factor SRSF10     autophagy     atherogenesis    

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Decitabine induces -mediated immune responses in p53-mutated triple-negative breast cancer: a clinical

《医学前沿（英文）》 doi: 10.1007/s11684-023-1016-8

摘要： p53 is mutated in half of cancer cases. However, no p53-targeting drugs have been approved. Here, we reposition decitabine for triple-negative breast cancer (TNBC), a subtype with frequent p53 mutations and extremely poor prognosis. In a retrospective study on tissue microarrays with 132 TNBC cases, DNMT1 overexpression was associated with p53 mutations (P = 0.037) and poor overall survival (OS) (P = 0.010). In a prospective DEciTabinE and Carboplatin in TNBC (DETECT) trial (NCT03295552), decitabine with carboplatin produced an objective response rate (ORR) of 42% in 12 patients with stage IV TNBC. Among the 9 trialed patients with available TP53 sequencing results, the 6 patients with p53 mutations had higher ORR (3/6 vs. 0/3) and better OS (16.0 vs. 4.0 months) than the patients with wild-type p53. In a mechanistic study, isogenic TNBC cell lines harboring DETECT-derived p53 mutations exhibited higher DNMT1 expression and decitabine sensitivity than the cell line with wild-type p53. In the DETECT trial, decitabine induced strong immune responses featuring the striking upregulation of the innate immune player IRF7 in the p53-mutated TNBC cell line (upregulation by 16-fold) and the most responsive patient with TNBC. Our integrative studies reveal the potential of repurposing decitabine for the treatment of p53-mutated TNBC and suggest IRF7 as a potential biomarker for decitabine-based treatments.

关键词： p53 mutation     triple-negative breast cancer     decitabine     DNMT1     IRF7     innate immune response    

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标题 作者 时间 类型 操作

RGS16 regulated by let-7c-5p promotes glioma progression by activating PI3K-AKT pathway

期刊论文

Novel variants in LAMA3 and COL7A1 and recurrent variant in KRT5 underlying epidermolysis bullosa in

期刊论文

A study on rapid acid chrome black (MB 7) spectrophotometric determination of ClO

Jing DONG, Huilong WANG

期刊论文

全球首例猪心脏移植人体手术

Sarah C. P. Williams

期刊论文

CRISPR基因编辑作物有望走上消费者的餐桌

Sarah C.P. Williams

期刊论文

地球工程研究从实验室走向现场

Sarah C.P. Williams

期刊论文

基因组学的发展助力古DNA研究

Sarah C.P. Williams

期刊论文

Non-thermal plasma for exhaust gases treatment

,Marquidia PACHECO P.,Fernando GÓMEZ B.,Joel PACHECO P.,Arturo COLÍN C.,José HUERTAS C.,Hilda FRÍAS P.

期刊论文

Novel mutation c.1210-3C>G in with a poly-T tract of 5T affects mRNA splicing in a Chinese patient

期刊论文

巨额资金将助推二氧化碳清除技术走向示范应用

Sarah C.P. Williams

期刊论文

Correlation between serum miR-154-5p and urinary albumin excretion rates in patients with type 2 diabetes

Huiwen Ren, Can Wu, Ying Shao, Shuang Liu, Yang Zhou, Qiuyue Wang

期刊论文

MicroRNA-142-3p and microRNA-142-5p are downregulated in hepatocellular carcinoma and exhibit synergistic

null

期刊论文

抗肥胖症药物市场需求旺盛

Sarah C. P. Williams

期刊论文

lncR-GAS5 upregulates the splicing factor to impair endothelial autophagy, leading to atherogenesis

期刊论文

Decitabine induces -mediated immune responses in p53-mutated triple-negative breast cancer: a clinical

期刊论文