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      • KCI등재

        MiR-873, as a suppressor in cervical cancer, inhibits cells proliferation, invasion and migration via negatively regulating ULBP2

        HaiXia Liang,Yu‑Hong Li 한국유전학회 2020 Genes & Genomics Vol.42 No.4

        Background Cervical cancer (CC) remains a large burden in the developing countries. The tumor inhibitory role of miR873 has been verified in a variety of cancers, however, whether miR-873 has a suppressive effect on CC remains unclear. Objective The purpose of this study was to investigate the functional role of miR-873 in CC, as well as explore the underlying molecular mechanism. Methods The prognostic values of miR-873 were assessed by Kaplan–Meier methods and cox regression models using the data which were downloaded from TCGA database. The expression of miR-873 was measured by RT-qPCR. Cell counting Kit-8, clone formation, and Transwell assays were used to assess the cell viability and metastasis, appropriately. The targeting relationship between miR-873 and ULBP2 was predicted by biological software and confirmed by dual luciferase reporter assay. Rescue assays were conducted to investigate whether miR-873 affects the phenotype of CC cells via regulating ULBP2. Results We observed that miR-873 was low-expressed in CC. Up-regulation of miR-873 notably restrained the proliferation, invasion and migration of C33a cells. Meanwhile, down-regulation of miR-873 in SiHa cells presented the opposite outcomes. ULBP2 was forecasted and certified as a target of miR-873. The results of rescue assays showed that overexpression of ULBP2 could restore the proliferation and motility of CC cells that inhibited by miR-873. Conclusion MiR-873 suppressed the CC cells proliferation, invasion and migration via negatively regulating ULBP2, suggesting that miR-873 could serve as a valuable therapeutic target for CC therapy.

      • The percolation threshold for tensile strength of polymer/CNT nanocomposites assuming filler network and interphase regions

        Li, Hai-xia,Zare, Yasser,Rhee, Kyong Yop Elsevier 2018 Materials chemistry and physics Vol.207 No.-

        <P><B>Abstract</B></P> <P>In this article, the percolation threshold for tensile strength of polymer/CNT nanocomposites (PCNT) is studied by known Pukanszky model. Since the network of nanoparticles forms at very low concentration of CNT, the filler network shows strengthening efficiency in PCNT beside the interphase regions surrounding nanoparticles. The Pukanszky model is developed by the properties of network such as density (N) and strength (σ<SUB>N</SUB>). The suggested equations are applied in some samples and the results are explained. Also, the effects of several parameters such as “N”, “σ<SUB>N</SUB>” and percolation volume fraction ( <SUB> ϕ p </SUB> ) on the strength of PCNT are plotted based on the developed model. The direct influences of “N” and “σ<SUB>N</SUB>” as well as the inverse effect of “ <SUB> ϕ p </SUB> ” on the tensile strength of PCNT are displayed. The “σ<SUB>N</SUB>” parameter only changes the strength of PCNT at low “ <SUB> ϕ p </SUB> ”, which shows the important role of percolation level.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Percolation threshold for tensile strength of polymer/CNT nanocomposites is studied. </LI> <LI> Filler network is a strengthening agent in PCNT beside the interphase. </LI> <LI> The suggested equations are applied in some samples and the results are explained. </LI> <LI> The effects of several parameters on the strength of PCNT are discussed. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

      • KCI등재

        The purified extract of steamed Panax ginseng protects cardiomyocyte from ischemic injury via caveolin-1 phosphorylation-mediating calcium influx

        Hai-Xia Li,Yan Ma,Yu-Xiao Yan,Xin-Ke Zhai,Meng-Yu Xin,Tian Wang,Dong-Cao Xu,Yu-Tong Song,Chun-Dong Song,Cheng-Xue Pan 고려인삼학회 2023 Journal of Ginseng Research Vol.47 No.6

        Background: Caveolin-1, the scaffolding protein of cholesterol-rich invaginations, plays an important rolein store-operated Ca2þ influx and its phosphorylation at Tyr14 (p-caveolin-1) is vital to mobilize protectionagainst myocardial ischemia (MI) injury. SOCE, comprising STIM1, ORAI1 and TRPC1, contributesto intracellular Ca2þ ([Ca2þ]i) accumulation in cardiomyocytes. The purified extract of steamed Panaxginseng (EPG) attenuated [Ca2þ]i overload against MI injury. Thus, the aim of this study was to investigatethe possibility of EPG affecting p-caveolin-1 to further mediate SOCE/[Ca2þ]i against MI injury in neonatalrat cardiomyocytes and a rat model. Methods: PP2, an inhibitor of p-caveolin-1, was used. Cell viability, [Ca2þ]i concentration were analyzedin cardiomyocytes. In rats, myocardial infarct size, pathological damages, apoptosis and cardiac fibrosiswere evaluated, p-caveolin-1 and STIM1 were detected by immunofluorescence, and the levels ofcaveolin-1, STIM1, ORAI1 and TRPC1 were determined by RT-PCR and Western blot. And, release of LDH,cTnI and BNP was measured. Results: EPG, ginsenosides accounting for 57.96%, suppressed release of LDH, cTnI and BNP, and protectedcardiomyocytes by inhibiting Ca2þ influx. And, EPG significantly relieved myocardial infarct size, cardiacapoptosis, fibrosis, and ultrastructure abnormality. Moreover, EPG negatively regulated SOCE viaincreasing p-caveolin-1 protein, decreasing ORAI1 mRNA and protein levels of ORAI1, TRPC1 and STIM1. More importantly, inhibition of the p-caveolin-1 significantly suppressed all of the above cardioprotectionof EPG. Conclusions: Caveolin-1 phosphorylation is involved in the protective effects of EPG against MI injury viaincreasing p-caveolin-1 to negatively regulate SOCE/[Ca2þ]i.

      • Clinical Significance of Upregulation of mir-196a-5p in Gastric Cancer and Enriched KEGG Pathway Analysis of Target Genes

        Li, Hai-Long,Xie, Shou-Pin,Yang, Ya-Li,Cheng, Ying-Xia,Zhang, Ying,Wang, Jing,Wang, Yong,Liu, Da-Long,Chen, Zhao-Feng,Zhou, Yong-Ning,Wu, Hong-Yan Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.5

        Background: miRNAs are relatively recently discovered cancer biomarkers which have important implications for cancer early diagnosis, treatment and estimation of prognosis. Here we focussed on expression of mir-196a-5p in gastric cancer tissues and cell lines so as to analyse its significance for clinicopathologic characteristics and generate enriched KEGG pathways clustered by target genes for exploring its potential roles as a biomarker in gastric cancer. Materials and Methods: The expression of mir-196a-5p in poorly, moderate and well differentiated gastric cancer cell lines compared with GES-1 was detected by RT-qPCR, and the expression of mir-196a-5p in gastric cancer tissues comparing with adjacent non cancer tissues of 58 cases were also assessed by RT-qPCR. Subsequently, an analysis of clinical significance of mir-196a-5p in gastric cancer and enriched KEGG pathways was executed based on the miRWalk prediction database combined with bioinformatics tools DAVID 6.7 and Mirfocus 3.0. Results: RT-qPCR showed that mir-196a-5p was up-regulated in 6 poorly and moderate differentiated gastric cancer cell lines SGC-7901, MKN-45, MKN-28, MGC-803, BGC-823, HGC-27 compared with GES-1, but down-regulated in the highly differentiated gastric cancer cell line AGS. Clinical data indicated mir-196a-5p to beup-regulated in gastric cancer tissues (47/58). Overexpression of mir-196a-5p was associated with more extensive degree of lymph node metastasis and clinical stage (P < 0.05; x2 test). Enriched KEGG pathway analyses of predicted and validated targets in miRWalk combined with DAVID 6.7 and Mirfocus 3.0 showed that the targeted genes regulated by mir-196a-5p were involved in malignancy associated biology. Conclusions: Overexpression of mir-196a-5p is associated with lymph node metastasis and clinical stage, and enriched KEGG pathway analyses showed that targeted genes regulated by mir-196a-5p may contribute to tumorgenesis, suggesting roles as an oncogenic miRNA biomarker in gastric cancer.

      • Malignant Transformation Rate and P53, and P16 Expression in Teratomatous Skin of Ovarian Mature Cystic Teratoma

        Zhu, Hai-Li,Zou, Zhen-Ning,Lin, Pei-Xin,Li, Wen-Xia,Huang, Ye-En,Shi, Xiao-Xin,Shen, Hong Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.3

        Objective: To investigate the incidence of malignant transformation and P53 and P16 expression in teratomatous skin of ovarian mature cystic teratoma. Materials and Methods: Data on ovarian teratoma specimens in nearly 10 years were reviewed. P53 and P16 expression were detected by immunohistochemistry in 25 cases of teratomatous skin of ovarian mature cystic teratoma, 20 cases of squamous cell carcinoma and 2 cases of squamous cell carcinoma originated from teratomatous skin. Results: Of 1913 cases of ovarian mature cystic teratoma in nearly 10 years, only two cases of squamous cell carcinoma were found in teratomatous skin, with malignant transformation rate of 0.1045%. P53 expression was detected in 2 cases squamous cell carcinoma originated from teratomatous skin and P16 overexpression in one. There were no expressions of P53 and P16 in 25 cases of teratomatous skin of ovarian mature cystic teratoma. Of 20 cases of squamous cell carcinoma P53 overexpression (positive rate of 55%) was detected in 11 cases, P16 overexpression (positive rate of 35%) in 7 cases. The positive rates of P53 and P16 expression in squamous cell carcinomas were significantly higher than that in the teratomatous skins (p< 0.001, p= 0.002). Conclusions: There was low risk of malignant transformation in teratomatous skin of ovarian mature cystic teratoma which can be explained by lower P53 and P16 expressionin teratomas than that in squamous cell carcinoma.

      • XPD Lys751Gln and Asp312Asn Polymorphisms and Susceptibility to Skin Cancer: A Meta-Analysis of 17 Case-control Studies

        Zhu, Hai-Li,Bao, Ji-Ming,Lin, Pei-Xin,Li, Wen-Xia,Zou, Zhen-Ning,Huang, Ye-En,Chen, Qing,Shen, Hong Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.16

        Background: Numerous studies have explored the influence of XPD Lys751Gln and/or Asp312Asn polymorphisms on skin cancer susceptibility. However, the results remain inconclusive. To derive a more precise estimation, we conducted a comprehensive search to identify all available published studies and performed a meta-analysis. Materials and Methods: Electronic literature searches of the PubMed, CBM and CNKI databases were performed up to March 2014. Odds ratios (ORs) with 95% confidence intervals (CIs) were applied to assess the strength of associations. Results: Seventeen case-control studies were included with a total sample size of 6, 113 cases and 11, 074 controls for the XPD Lys751Gln polymorphism, and 10 studies (3, 840cases and 7, 637 controls) for the XPD Asp312Asn polymorphism were pooled for analysis. Overall, no significant associations were found between the XPD Lys751Gln polymorphism and skin cancer risk in any genetic model. On stratified analysis by tumor type, XPD Lys751Gln polymorphism was not associated with increased risk of non-melanoma skin cancer, but was significantly related with increased risk of cutaneous melanoma (Gln/Gln vs Lys/Lys: OR=1.15, 95%CI=1.02-1.29, p=0.023; dominant model: OR=1.09, 95%CI=1.01-1.18, p=0.036). For the XPD Asp312Asn polymorphism, no significant association with skin cancer risk was observed in overall or subgroup analyses. Conclusions: The present meta-analysis suggests that the XPD Lys751Gln polymorphism may contribute to the risk of cutaneous melanoma from currently available evidence. Further investigations are needed to obtain more insight into possible roles of these two polymorphisms in skin carcinogenesis.

      • KCI등재

        Cordblood-Based High-Throughput Screening for Deafness Gene of 646 Newborns in Jinan Area of China

        Shou-Xia Li,Ding-Li Chen,Su-Bin Zhao,Li-Li Guo,Hai-Qin Feng,Xiao-Fang Zhang,Li-Li Ping,Zhi-Ming Yang,Cai-Xia Sun,Gen-Dong Yao 대한이비인후과학회 2015 Clinical and Experimental Otorhinolaryngology Vol.8 No.3

        Objectives. Infants with slight/mild or late-onset hearing impairment might be missed in universal newborn hearing screening (UNHS). We identified the mutation hot spot of common deaf gene in the newborns in Jinan area population by screening the mutation spot with neonate cord blood, in order to make clear whether the neonate cord blood for screening is feasible. Methods. Six hundred and forty-six newborns were subjected to both UNHS and genetic screening for deafness by using neonate cord blood. The newborn genetic screening targeted four deafness-associated genes, which were commonly found in the Chinese population including gap junction beta-2 protein (GJB2), gap junction beta-3 protein (GJB3), solute carrier family 26 member 4 (SLC26A4), and mtDNA 12S rRNA. The most common 20 spot mutations in 4 deaf genes were detected by MassARRAY iPLEX platform and mitochondrial 12S rRNA A1555G and C1494T mutations were sequenced using Sanger sequencing. Results. Among the 646 newborns, 635 cases passed the UNHS and the other 11 cases (1.7%) did not. Of the 11 failures, two cases were found to carry homozygous GJB2 p.R143W pathogenic mutation, one case was found to have heterozygous GJB2 235delC mutation, and another one case carried heterozygous GJB3 p.R180X pathogenic mutation. Six hundred and thirty-five babies passed the newborn hearing screening, in which 25 babies were identified to carry pathogenic mutations, including 12 heterozygotes (1.9%) for GJB2 235delC, eight heterozygotes (1.3%) for SLC26A4 IVS7-2A>G, one heterozygote (0.2%) for p.R409H, two homozygotes (0.3%) for m.1494C>T, and two homozygotes (0.3%) for m.1555A>G. Conclusion. Newborn genetic screening through the umbilical cord blood for common deafness-associated mutations may identify carriers sensitive to aminoglycoside antibiotic, and can effectively prevent or delay hearing loss occurs.

      • KCI등재

        Liposomal honokiol, a potent anti-angiogenesis agent, in combination with radiotherapy produces a synergistic antitumor efficacy without increasing toxicity

        Jia Hu,Li Liu,Xiang Chen,Ping Chen,Guang-li Yang,Wen-li Hou,Ming-hai Tang,Fan Zhang,Xian-huo Wang,Xia Zhao,Yu-quan Wei,Li-juan Chen 생화학분자생물학회 2008 Experimental and molecular medicine Vol.40 No.6

        Honokiol is an active compound purified from magnolia that has been shown to induce cell differentiation, apoptosis, and anti-angiogenesis effects, as well as an enhancement in tumor growth delay in combination with chemotherapeutic agents in several mouse xenograft models. Our goal was to investigate the radiosensitization effect of honokiol on lung carcinoma. The radiosensitization effect of liposomal honokiol in Lewis lung carcinoma cells (LL/2) was analyzed using an in vitro clonogenic survival assay. For an in vivo study, Lewis lung carcinoma-bearing C57BL/6 mice were treated with either liposomal honokiol at 25 mg/kg or 5 Gy of single tumor radiation, or a combination of both over 12 days of treatment. The tumor growth delay and the survival time were evaluated. In addition, histological analysis of tumor sections was performed to examine changes by detecting the microvessel density and apoptosis in tumor tissues. In the clonogenic survival assay, LL/2 cells treated with IC50 Lipo-HNK for 24 h showed a radiation enhancement ratio of 1.9. After 12 days of combination treatment, the tumor volume decreased 78% and produced an anti-tumor activity 1.3-fold greater than a predicted additive effect of honokiol and radiation alone. This combination treatment also caused an 8.7 day delay in tumor growth. The cell cycle distribution and histological analysis demonstrated that liposomal honokiol has an anti-tumor effect via inducing apoptosis and inhibiting angiogenesis. Liposomal honokiol can enhance tumor cell radiosensitivity in vitro and in vivo, indicating that radiotherapy combined with liposomal honokiol can lead to greater anti-tumor efficacy. Honokiol is an active compound purified from magnolia that has been shown to induce cell differentiation, apoptosis, and anti-angiogenesis effects, as well as an enhancement in tumor growth delay in combination with chemotherapeutic agents in several mouse xenograft models. Our goal was to investigate the radiosensitization effect of honokiol on lung carcinoma. The radiosensitization effect of liposomal honokiol in Lewis lung carcinoma cells (LL/2) was analyzed using an in vitro clonogenic survival assay. For an in vivo study, Lewis lung carcinoma-bearing C57BL/6 mice were treated with either liposomal honokiol at 25 mg/kg or 5 Gy of single tumor radiation, or a combination of both over 12 days of treatment. The tumor growth delay and the survival time were evaluated. In addition, histological analysis of tumor sections was performed to examine changes by detecting the microvessel density and apoptosis in tumor tissues. In the clonogenic survival assay, LL/2 cells treated with IC50 Lipo-HNK for 24 h showed a radiation enhancement ratio of 1.9. After 12 days of combination treatment, the tumor volume decreased 78% and produced an anti-tumor activity 1.3-fold greater than a predicted additive effect of honokiol and radiation alone. This combination treatment also caused an 8.7 day delay in tumor growth. The cell cycle distribution and histological analysis demonstrated that liposomal honokiol has an anti-tumor effect via inducing apoptosis and inhibiting angiogenesis. Liposomal honokiol can enhance tumor cell radiosensitivity in vitro and in vivo, indicating that radiotherapy combined with liposomal honokiol can lead to greater anti-tumor efficacy.

      • Lack of Prognostic Value of Human Epidermal Growth Factor- Like Receptor 2 Status in Inflammatory Breast Cancer (IBC): a Meta-analysis

        Li, Xiu-Juan,Zha, Quan-Bin,Xu, Xin-Yu,Xia, Lei,Zhang, Zhe,Ren, Zhao-Jun,Tang, Jin-Hai Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.22

        Inflammatory breast cancer (IBC) is a rare, aggressive form of breast cancer which is more likely to be her-2/neu amplified. While the her-2/neu status has been utilised to predict prognosis, the published data are inconsistent. The present meta-analysis was conducted to determine whether the her-2/neu status predicts outcomes. Papers were selected from the PubMed database based on defined inclusion and exclusion criteria. Parameters such as total patients, follow-up time and outcome statistics (i.e. overall survival (OS), relapse-free survival (RFS) were collected. The analysis included 6 studies with 2,838 IBC patients. The summary hazards ratio (HR) estimating the association of OS with HER-2-positive disease was 0.96 (95% confidence interval (95%CI: 0.85-1.10)), with similar findings for RFS (HR=0.81, 95%CI: 0.61-1.09). No obvious statistical heterogeneity was detected. This meta-analysis suggests that HER-2-positive status is not an independent adverse prognostic factor for survival among IBC patient cases.

      • KCI등재

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