Molecular characterization of the sans fille gene in Antheraea pernyi: A highly conserved gene during the evolution of animals

Ya-Jie Li,Rui Mi,Nan Meng,Zhi-Xin Wen,Xue-Jun Li,Mo Chen,Yan-Qun Liu,Shu-Ying Li 한국응용곤충학회 2013 Journal of Asia-Pacific Entomology Vol.16 No.3

Sans-fille (SNF) is the Drosophila homologue ofmammalian general splicing factors U1A and U2B″, and plays an important role in sex determination in Drosophilamelanogaster. In this study, the snf gene fromAntheraea pernyi (Lepidoptera: Saturniidae), an economically important insect, was isolated and characterized. The obtained 925 bp cDNA sequence contains an open reading frame of 669 bp encoding a polypeptide of 222 amino acids,showing 78% sequence identity to that from D. melanogaster. A database search revealed that SNF protein homologs are present in many animals, including invertebrates and vertebrates, with more than 70% amino acid sequence identities, suggesting that they were highly conserved during the evolution of animals. Phylogenetic analysis revealed that A. pernyi SNF was closely related to Bombyx mori SNF. Quantitative real-time PCR (qRT-PCR) analysis showed that the A. pernyi snf gene was transcribed during five larval developmental stages,and in six tested tissues (ovaries, testes, silk glands, fat body, integument, and hemolymph),with the most abundance determined in the gonads (ovaries or testes). Investigation of expression changes throughout embryonic development indicated that A. pernyi snfmRNAwas expressed at a lowlevel fromdays 0 to 4, and reached amaximum level at day 10, but decreased to a low level before hatching. These results suggest that the product of the snf gene may play important roles in the development of A. pernyi.

Eukaryotic Translation Initiation Factor 3a (eIF3a) Promotes Cell Proliferation and Motility in Pancreatic Cancer

Shu-qian Wang,Yu Liu,Min-ya Yao,Jing Jin 대한의학회 2016 Journal of Korean medical science Vol.31 No.10

Identifying a target molecule that is crucially involved in pancreatic tumor growth and metastasis is necessary in developing an effective treatment. The study aimed to investigate the role of the eukaryotic translation initiation factor 3a (eIF3a) in the cell proliferation and motility in pancreatic cancer. Our data showed that the expression of eIF3a was upregulated in pancreatic ductal adenocarcinoma as compared with its expression in normal pancreatic tissues. Knockdown of eIF3a by a specific shRNA caused significant decreases in cell proliferation and clonogenic abilities in pancreatic cancer SW1990 and Capan-1 cells. Consistently, the pancreatic cancer cell growth rates were also impaired in xenotransplanted mice. Moreover, wound-healing assay showed that depletion of eIF3a significantly slowed down the wound recovery processes in SW1990 and Capan-1 cells. Transwell migration and invasion assays further showed that cell migration and invasion abilities were significantly inhibited by knockdown of eIF3a in SW1990 and Capan-1 cells. Statistical analysis of eIF3a expression in 140 cases of pancreatic ductal adenocarcinoma samples revealed that eIF3a expression was significantly associated with tumor metastasis and TNM staging. These analyses suggest that eIF3a contributes to cell proliferation and motility in pancreatic ductal adenocarcinoma.

Fatty Acid Binding Protein 5 (FABP5) Promotes Aggressiveness of Gastric Cancer Through Modulation of Tumor Immunity

Shu Zhang,Mei-qing Qiu,Hui-jun Wang,Ya-fei Ju,Zhen Liu,Tao Wang,Shi-feng Kan,Zhen Yang,Ya-yun Cui,You-qiang Ke,Hong-min He,Li Sun 대한위암학회 2023 Journal of gastric cancer Vol.23 No.2

Purpose: Gastric cancer (GC) is the second most lethal cancer globally and is associated with poor prognosis. Fatty acid-binding proteins (FABPs) can regulate biological properties of carcinoma cells. FABP5 is overexpressed in many types of cancers; however, the role and mechanisms of action of FABP5 in GC remain unclear. In this study, we aimed to evaluate the clinical and biological functions of FABP5 in GC. Materials and Methods: We assessed FABP5 expression using immunohistochemical analysis in 79 patients with GC and evaluated its biological functions following in vitro and in vivo ectopic expression. FABP5 targets relevant to GC progression were determined using RNA sequencing (RNA-seq). Results: Elevated FABP5 expression was closely associated with poor outcomes, and ectopic expression of FABP5 promoted proliferation, invasion, migration, and carcinogenicity of GC cells, thus suggesting its potential tumor-promoting role in GC. Additionally, RNA-seq analysis indicated that FABP5 activates immune-related pathways, including cytokine-cytokine receptor interaction pathways, interleukin-17 signaling, and tumor necrosis factor signaling, suggesting an important rationale for the possible development of therapies that combine FABP5-targeted drugs with immunotherapeutics. Conclusions: These findings highlight the biological mechanisms and clinical implications of FABP5 in GC and suggest its potential as an adverse prognostic factor and/or therapeutic target.

Employee Stress, Job Satisfaction, and Job Performance: A Comparison between High-technology and Traditional Industry in Taiwan

YANG, Shu Ya,CHEN, Shui Chuan,LEE, Liza,LIU, Ying Sing Korea Distribution Science Association 2021 The Journal of Asian Finance, Economics and Busine Vol.8 No.3

The use of human resources determines the success of enterprises. This study applies the questionnaire design method to analyze the relationship between job stress, job satisfaction, and job performance, noting that few studies have comparatively examined these variables between industries, especially between high-tech and traditional industries. The proposed assessment model in this study can facilitate decision-makers' ability to make the optimal business decisions through their personnel systems, thereby improving employee satisfaction and increasing job performance. This study found that in the traditional and high-tech industries, some demographic variables have significant differences in the job stress, job satisfaction and job performance, but the demographic variables that can significantly affect the differences in these job's variables are differences between industries. This study acknowledges that job stress and performance have a significantly negative correlation, and traditional industries will have more stress factors than high-tech industries. In addition, support for traditional industries exist in job satisfaction and performance has a significantly positive correlation, but not in high-tech industries. Job stress for performance has a significantly negative correlation in two industries. This study reconfirmed the relationship between job stress, satisfaction and performance, found some differences in this relationship and the respective industrial characteristics.

Increased Serotonin Signaling Contributes to the Warburg Effect in Pancreatic Tumor Cells Under Metabolic Stress and Promotes Growth of Pancreatic Tumors in Mice

Jiang, Shu-Heng,Li, Jun,Dong, Fang-Yuan,Yang, Jian-Yu,Liu, De-Jun,Yang, Xiao-Mei,Wang, Ya-Hui,Yang, Min-Wei,Fu, Xue-Liang,Zhang, Xiao-Xin,Li, Qing,Pang, Xiu-Feng,Huo, Yan-Miao,Li, Jiao,Zhang, Jun-Feng Elsevier 2017 Gastroenterology Vol.153 No.1

<P><B>Background & Aims</B></P> <P>Desmoplasia and poor vascularity cause severe metabolic stress in pancreatic ductal adenocarcinomas (PDACs). Serotonin (5-HT) is a neuromodulator with neurotransmitter and neuroendocrine functions that contributes to tumorigenesis. We investigated the role of 5-HT signaling in the growth of pancreatic tumors.</P> <P><B>Methods</B></P> <P>We measured the levels of proteins that regulate 5-HT synthesis, packaging, and degradation in pancreata from Kras<SUP>G12D/+</SUP>/Trp53<SUP>R172H/+</SUP>/Pdx1-Cre (KPC) mice, which develop pancreatic tumors, as well as in PDAC cell lines and a tissue microarray containing 81 human PDAC samples. We also analyzed expression levels of proteins involved in 5-HT synthesis and degradation by immunohistochemical analysis of a tissue microarray containing 311 PDAC specimens, and associated expression levels with patient survival times. 5-HT level in 14 matched PDAC tumor and non-tumor tissues were analyzed by ELISA. PDAC cell lines were incubated with 5-HT and cell survival and apoptosis were measured. We analyzed expression of the 5-HT receptor HTR2B in PDAC cells and effects of receptor agonists and antagonists, as well as HTR2B knockdown with small hairpin RNAs. We determined the effects of 5-HT stimulation on gene expression profiles of BxPC-3 cells. Regulation of glycolysis by 5-HT signaling via HTR2B was assessed by immunofluorescence and immunoprecipitation analyses, as well as by determination of the extracellular acid ratio, glucose consumption, and lactate production. Primary PDACs, with or without exposure to SB204741 (a selective antagonist of HTR2B), were grown as xenograft tumors in mice, and SB204741 was administered to tumor-bearing KPC mice; tumor growth and metabolism were measured by imaging analyses.</P> <P><B>Results</B></P> <P>In immunohistochemical analysis of a tissue microarray of PDAC specimens, increased levels of TPH1 and decreased level of MAOA, which regulate 5-HT synthesis and degradation, correlated with stage and size of PDACs and shorter patient survival time. We found levels of 5-HT to be increased in human PDAC tissues compared with non-tumor pancreatic tissues, and PDAC cell lines compared with non-transformed pancreatic cells. Incubation of PDAC cell lines with 5-HT increased proliferation and prevented apoptosis. Agonists of HTR2B, but not other 5-HT receptors, promoted proliferation and prevented apoptosis of PDAC cells. Knockdown of HTR2B in PDAC cells, or incubation of cells with HTR2B inhibitors, reduced their growth as xenograft tumors in mice. We observed a correlation between 5-HT and glycolytic flux in PDAC cells; levels of metabolic enzymes involved in glycolysis, the phosphate pentose pathway, and hexosamine biosynthesis pathway increased significantly in PDAC cells following 5-HT stimulation. 5-HT stimulation led to formation of the HTR2B–LYN–p85 complex, which increased PI3K–Akt–mTOR signaling and the Warburg effect by increasing protein levels of MYC and HIF1A. Administration of SB204741 to KPC mice slowed growth and metabolism of established pancreatic tumors and prolonged survival of the mice.</P> <P><B>Conclusions</B></P> <P>Human PDACs have increased levels of 5-HT, and PDAC cells increase expression of its receptor, HTR2B. These increases allow for tumor glycolysis under metabolic stress and promote growth of pancreatic tumors and PDAC xenograft tumors in mice.</P>

The Short-Term Fear Effects for Taiwan's Equity Market from Bad News Concerning Sino-U.S. Trade Friction

YANG, Shu Ya,LIN, Hsiu Hsu,LIU, Ying Sing Korea Distribution Science Association 2021 The Journal of Asian Finance, Economics and Busine Vol.8 No.3

Mainland China area has been a long-term, major trade rival and partner of Taiwan, accounting for more than 40% of Taiwan's total annual trade exports, and so Sino-US trade friction is expected to have a significant impact on Taiwan's economy in the future. This study focuses on major bad news of Sino-US trade frictions and how it generates short-term shocks for Taiwan's equity market and fear sentiment. It further explores the mutual interpretation relationship between price changes such as VIX, Taiwan's stock market index, and the VIX ETF to identify which factors have information leadership as leading indicators. The study period covers 750 trading days from 2017/1/3 to 2020/1/31. This study finds that, when a policy news is announced, the stock market index falls significantly, the change in the trading price (net value) of the VIX ETF rises significantly, and the overprice rate significantly drops, but VIX does not, showing that fear sentiment exists in the Taiwan's market. The net value of the VIX ETF shows an information advantage as a leading indicator. This study suggests that, when the world's two largest economies clash over trade, the impact on Taiwan's equity market is inevitable, and that short-term fear effects will arise.

Hsa-let-7c controls the committed differentiation of IGF-1-treated mesenchymal stem cells derived from dental pulps by targeting IGF-1R via the MAPK pathways

Gen-Xia Liu,Shu Ma,Yao Li,Yan Yu,Yi-Xiang Zhou,Ya-Die Lu,Lin Jin,Zi-Lu Wang,Jin-Hua Yu 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-

The putative tumor suppressor microRNA let-7c is extensively associated with the biological properties of cancer cells. However, the potential involvement of let-7c in the differentiation of mesenchymal stem cells has not been fully explored. In this study, we investigated the influence of hsa-let-7c (let-7c) on the proliferation and differentiation of human dental pulp-derived mesenchymal stem cells (DPMSCs) treated with insulin-like growth factor 1 (IGF-1) via flow cytometry, CCK-8 assays, alizarin red staining, real-time RT-PCR, and western blotting. In general, the proliferative capabilities and cell viability of DPMSCs were not significantly affected by the overexpression or deletion of let-7c. However, overexpression of let-7c significantly inhibited the expression of IGF-1 receptor (IGF-1R) and downregulated the osteo/odontogenic differentiation of DPMSCs, as indicated by decreased levels of several osteo/odontogenic markers (osteocalcin, osterix, runt-related transcription factor 2, dentin sialophosphoprotein, dentin sialoprotein, alkaline phosphatase, type 1 collagen, and dentin matrix protein 1) in IGF-1-treated DPMSCs. Inversely, deletion of let- 7c resulted in increased IGF-1R levels and enhanced osteo/odontogenic differentiation. Furthermore, the ERK, JNK, and P38 MAPK pathways were significantly inhibited following the overexpression of let-7c in DPMSCs. Deletion of let-7c promoted the activation of the JNK and P38 MAPK pathways. Our cumulative findings indicate that Let-7c can inhibit the osteo/odontogenic differentiation of IGF-1-treated DPMSCs by targeting IGF-1R via the JNK/P38 MAPK signaling pathways.

RON and MET Co-overexpression Are Significant Pathological Characteristics of Poor Survival and Therapeutic Targets of Tyrosine Kinase Inhibitors in Triple-Negative Breast Cancer

Tian-Hao Weng,Min-Ya Yao,Xiang-Ming Xu,Chen-Yu Hu,Shu-Hao Yao,Yi-Zhi Liu,Zhi-Gang Wu,Tao-Ming Tang,Pei-Fen Fu,Ming-Hai Wang,Hang-Ping Yao 대한암학회 2020 Cancer Research and Treatment Vol.52 No.3

Purpose Triple-negative breast cancer (TNBC) is highly malignant and has poor prognosis and a high mortality rate. The lack of effective therapy has spurred our investigation of new targets for treating this malignant cancer. Here, we identified RON (macrophage-stimulating 1 receptor) and MET (MET proto-oncogene, receptor tyrosine kinase) as a prognostic biomarker and therapeutic targets for potential TNBC treatment. Materials and Methods We analyzed RON and MET expression in 187 primary TNBC clinical samples with immunohistochemistry. We validated the targeted therapeutic effects of RON and MET in TNBC using three tyrosine kinase inhibitors (TKIs): BMS-777607, INCB28060, and tivantinib. The preclinical therapeutic efficacy of the TKIs was mainly estimated using a TNBC xenograft model. Results Patients with TNBC had widespread, abnormal expression of RON and MET. There was RON overexpression, MET overexpression, and RON and MET co-overexpression in 63 (33.7%), 63 (33.7%), and 43 cases (23.0%), respectively, which had poor prognosis and short survival. In vivo, the TKI targeting RON ant MET inhibited the activation of the downstream signaling molecules, inhibited TNBC cell migration and proliferation, and increased TNBC cell apoptosis; in the xenograft model, they significantly inhibited tumor growth and shrank tumor volumes. The TKI targeting RON and Met, such as BMS-777607 and tivantinib, yielded stronger anti-tumor effects than INCB28060. Conclusion RON and MET co-overexpression can be significant pathological characteristics in TNBC for poor prognosis. TKIs targeting RON and MET have stronger drug development potential for treating TNBC.

Adherence to Cancer Prevention Guidelines and Endometrial Cancer Risk: Evidence from a Systematic Review and Dose-Response Meta-analysis of Prospective Studies

Hui Sun,Qing Chang,Ya-Shu Liu,Yu-Ting Jiang,Ting-Ting Gong,Xiao-Xin Ma,Yu-Hong Zhao,Qi-Jun Wu 대한암학회 2021 Cancer Research and Treatment Vol.53 No.1

Purpose The evidence of adherence to cancer prevention guidelines and endometrial cancer (EC) risk has been limited and controversial. This study summarizes and quantifies the relationship between adherence to cancer prevention guidelines and EC risk. Materials and Methods The online databases PubMed, Web of Science, and EMBASE were searched for relevant publications up to June 2, 2020. This study had been registered at PROSPERO. The registration number is CRD42020149966. Study quality evaluation was performed based on the Newcastle-Ottawa Scale. The I2 statistic was used to estimate heterogeneity among studies. Egger’s and Begg’s tests assessed potential publication bias. Summary hazard ratios (HRs) and 95% confi dence intervals (CIs) for the relationship between adherence to cancer prevention guidelines score was assigned to participants by summarizing individual scores for each lifestyle-related factor. The scores ranged from least healthy (0) to most healthy (20) and the EC risk was calculated using a random-effects model. Results Five prospective studies (four cohort studies and one case‑cohort study) consisted of 4,470 EC cases, where 597,047 participants were included. Four studies had a low bias risk and one study had a high bias risk. Summary EC HR for the highest vs. lowest score of adherence to cancer prevention guidelines was 0.54 (95% CI, 0.40 to 0.73) and had a high heterogeneity (I2=86.1%). For the dose-response analysis, an increment of 1 significantly reduced the risk of EC by 6%. No signifi cant publication bias was detected. Conclusion This study suggested that adherence to cancer prevention guidelines was negatively related to EC risk.

Health-related Quality of Life among Breast Cancer Patients and its Influencing Factor in a Chinese Population

Shen, Fang-Rong,Liu, Ming,Zhang, Xia,Feng, Ya-Hong,Zhou, Long-Shu,Chen, You-Guo Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.8

Aim: The aim of this study was to investigate the quality of life (QOL) of breast cancer patients by using the Functional Assessment of Cancer Therapy-Breast (FACT-B) questionnaires. Methods: A total of 522 adult patients who were admitted to our hospital with breast cancer were collected during the period of Jun. 2007 to Dec. 2009. Results: Our FACT-B questionnaire study suggested that women below 50 years old, employed, higher education and annual income, lower TNM stage and receiving modified radical mastectomy manifested significantly better QOL using the assessment tool of the FACT-B subscale. Moreover, regression analysis indicated patients with young age, low stage cancer, high education and income were more likely to have high score of QOL, with ORs (95% CI) of 2.8 (1.52-4.56), 2.1 (1.15-3.95), 3.1 (1.45-5.12) and 3.54 (1.54-5.43), respectively. Conclusions: Our study showed younger age, lower stage of cancer, higher education and income could influence the QOL of breast cancer patients in our Chinese population. Further large sample studies are still needed for confirmation.