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RISS 인기검색어
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- 저자 : Jin Yucui (검색결과 4 건)
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Association of polymorphisms in Pit-1 gene with growth and feed efficiency in meat-type chickens
Sihua Jin,Tingting He,Lei Yang,Yucui Tong,Xingyong Chen,Zhaoyu Geng 아세아·태평양축산학회 2018 Animal Bioscience Vol.31 No.11
Objective: The pituitary specific transcription factor-1 (Pit-1) gene is responsible for pituitary development and growth hormone expression and is regarded as a pivotal candidate gene for growth and production in chickens. Therefore, the aim of this study was to investigate the association of Pit-1 polymorphisms with growth and feed efficiency traits in yellow meat-type chickens. Methods: In the present study, five single nucleotide polymorphisms (SNPs) of Pit-1 were selected and genotyped by high-throughput matrix-assisted laser desorption-ionization time-of-flight mass spectrometry in 724 meat-type chickens. Results: Association analysis showed that rs13687126 of Pit-1 was strongly associated with body weight gain (BWG) and feed intake (FI) (p<0.05), and that rs13687128 was significantly correlated with body weight at 70 days of age (BW70), BWG and feed conversion ratio (FCR) (p<0.05). SNP rs13905622 was strongly related to BW70 and FCR (p<0.05). Furthermore, birds with the GG genotype of rs13687126 had larger BWG and FI than those with the AG genotype (p<0.05). Individuals with the TT genotype of rs13687128 were significantly higher BW70 and BWG than those of the CT and CC genotype, while FCR was just the opposite (p<0.05). For rs13905622, the AA chickens showed strongly larger BW70 and lower FCR compared with the AT and TT chickens (p<0.05). Additionally, an ACA haplotype based on rs13687126, rs13687128, and rs13905622 had significant effects on BW70 and FCR (p<0.05). Conclusion: Our studies thus provide crucial evidence for the relationship between polymorphisms of Pit-1 and growth and feed efficiency traits which may be useful for meat-type chicken breeding programs.
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TFPI inhibits breast cancer progression by suppressing ERK/p38 MAPK signaling pathway
Xing Mengying,Yang Ying,Huang Jiaxue,Fang Yaqun,Jin Yucui,Li Lingyun,Chen Xiang,Zhu Xiaoxia,Ma Changyan 한국유전학회 2022 Genes & Genomics Vol.44 No.7
Background: Tissue factor pathway inhibitor-1 (TFPI) is a serine protease inhibitor, which is responsible for inactivating TF-induced coagulation. Recently, increasing studies revealed that TFPI was lowly expressed in tumor cells and exhibited the antitumor activity. Objective: The aim of this study was to explore the role and underlying molecular mechanisms of TFPI in breast cancer. Methods: The expression and prognostic value of TFPI were analyzed using UALCAN and Kaplan-Meier plotter website. The expression level of TFPI in breast cancer tissues and cells was examined by immunohistochemistry (IHC) and western blot analysis, respectively. Cellular proliferation was evaluated by CCK-8 and colony formation assays. Cell migration and invasion were determined by transwell assay. The methylation level of TFPI promoter was determined by methylation-specific PCR. Results: TFPI expression was significantly lower in breast cancer tissues and cells compared to normal breast tissues and normal breast cells. Patients with low TFPI levels showed worse overall survival (OS). Furthermore, overexpression of TFPI significantly inhibited the proliferation, migration and invasion of breast cancer cells. Conversely, knockdown of TFPI promoted the proliferation, migration and invasion of breast cancer cells. Mechanistically, TFPI inhibited the ERK/p38 MAPK signaling pathway in breast cancer. Moreover, DNA hypermethylation of TFPI promoter was responsible for the downregulation of TFPI in breast cancer cells. Conclusion: TFPI inhibited breast cancer cell proliferation, migration and invasion through inhibition of the ERK/p38 MAPK signaling pathway, suggesting that TFPI may serve as a novel prognostic biomarker and therapeutic target for breast cancer.
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Yang Jiashu,Zhang Ming,Yang Dawei,Ma Yunfei,Tang Yuting,Xing Mengying,Li Lingyun,Chen Li,Jin Yucui,Ma Changyan 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-
Long noncoding RNAs (lncRNAs) have emerged as important regulators of osteoarthritis (OA), but the biological roles and clinical significance of most lncRNAs in OA are not fully understood. Microarray analysis was performed to identify differentially expressed lncRNAs, mRNAs, and miRNAs between normal and osteoarthritic cartilage. We found that AC008440.5 (abbreviated AC008), as well as AQP1 and ANKH, were highly expressed in osteoarthritic cartilage, whereas miR-328-3p was expressed at a low level in osteoarthritic cartilage. Functional assays showed that ectopic expression of AC008, AQP1, and ANKH significantly decreased chondrocyte viability and promoted chondrocyte apoptosis and extracellular matrix (ECM) degradation, whereas knockdown of AC008, AQP1, and ANKH resulted in the opposite effects. Moreover, miR-328-3p overexpression increased chondrocyte viability and attenuated chondrocyte apoptosis and ECM degradation, whereas inhibition of miR-328-3p resulted in the opposite effects. Bioinformatics analysis, RNA immunoprecipitation (RIP), and luciferase assays revealed that AC008 functioned as a competing endogenous RNA (ceRNA) to regulate miR-328-3p, which specifically targeted the AQP1 and ANKH genes. In addition, miR-328-3p significantly ameliorated MIA-induced OA, whereas AC008 accelerated OA progression in vivo. Furthermore, fat mass and obesity-associated (FTO)-mediated N6-methyladenosine demethylation downregulated AC008 transcription, while lower FTO expression led to upregulation of AC008 transcription in OA. In conclusion, our data reveal that AC008 plays a critical role in OA pathogenesis via the miR-328-3p‒AQP1/ANKH pathway, suggesting that AC008 may be a potential therapeutic target for OA.
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