Long Noncoding RNA HOXA11-AS Modulates the Resistance of Nasopharyngeal Carcinoma Cells to Cisplatin via miR-454-3p/c-Met

Feng-Jie Lin,Xian-Dong Lin,Lu-Ying Xu,Shi-Quan Zhu 한국분자세포생물학회 2020 Molecules and cells Vol.43 No.10

To elucidate the mechanism of action of HOXA11-AS in modulating the cisplatin resistance of nasopharyngeal carcinoma (NPC) cells. HOXA11-AS and miR-454-3p expression in NPC tissue and cisplatin-resistant NPC cells were measured via quantitative reverse transcriptase polymerase chain reaction. NPC parental cells (C666-1 and HNE1) and cisplatin-resistant cells (C666-1/DDP and HNE1/DDP) were transfected and divided into different groups, after which the MTT method was used to determine the inhibitory concentration 50 (IC50) of cells treated with different concentrations of cisplatin. Additionally, a clone formation assay, flow cytometry and Western blotting were used to detect DDP-induced changes. Thereafter, xenograft mouse models were constructed to verify the in vitro results. Obviously elevated HOXA11-AS and reduced miR-454-3p were found in NPC tissue and cisplatin-resistant NPC cells. Compared to the control cells, cells in the si-HOXA11-AS group showed sharp decreases in cell viability and IC50, and these results were reversed in the miR-454-3p inhibitor group. Furthermore, HOXA11-AS targeted miR-454-3p, which further targeted c-Met. In comparison with cells in the control group, HNE1/DDP and C666-1/DDP cells in the si-HOXA11-AS group demonstrated fewer colonies, with an increase in the apoptotic rate, while the expression levels of c-Met, p-Akt/Akt and p-mTOR/mTOR decreased. Moreover, the si-HOXA11-AS-induced enhancement in sensitivity to cisplatin was abolished by miR-454-3p inhibitor transfection. The in vivo experiment showed that DDP in combination with si-HOXA11-AS treatment could inhibit the growth of xenograft tumors. Silencing HOXA11-AS can inhibit the c-Met/AKT/mTOR pathway by specifically upregulating miR-454-3p, thus promoting cell apoptosis and enhancing the sensitivity of cisplatin-resistant NPC cells to cisplatin.

Inverse Analysis of Inconel 718 Laser-Assisted Milling to Achieve Machined Surface Roughness

Yixuan Feng,Tsung-Pin Hung,Yu-Ting Lu,Yu-Fu Lin,Fu-Chuan Hsu,Chiu-Feng Lin,Ying-Cheng Lu,Xiaohong Lu,Steven Y. Liang 한국정밀공학회 2018 International Journal of Precision Engineering and Vol.19 No.11

This manuscript proposes an inverse analysis method for the machined surface roughness in laser-assisted milling on Inconel 718. The method solves the forward problem considering the tool profile and the elastic recovery of machined surface and applies the variance-based recursive method to guide the updating mechanism of process parameters to match the measurements. Subsequently, the inverse analysis identifies four process parameters of feed per tooth, tool tip radius, minimum cutting thickness, and tool tip angle, and finds the optimal solution for target performance, the surface roughness. The measurements are collected under the single beam coaxial laser-assisted milling spindle. The proposed modified Kalman filter algorithm introduces the gain coefficient G when updating the process parameters to improve robustness and accuracy. The inverse analysis is conducted on all measurements, and the average error of target performance is 0.460% when the laser is on and 0.394% when the laser is off. The average difference of process parameters is less than 5%, and the selection process is done in 50 loops within a minute. Therefore, the proposed inverse analysis model is robust, adaptive to different initial guesses and measurements, highly accurate, and saves computation time.

Autophagy plays a protective role against apoptosis induced by toxicarioside N via the Akt/mTOR pathway in human gastric cancer SGC-7901 cells

Huan-ge Zhao,Song-lin Zhou,Ying-ying Lin,Hua Wang,Hao Fu Dai,Feng-Ying Huang 대한약학회 2018 Archives of Pharmacal Research Vol.41 No.10

Toxicarioside N (Tox N), a natural product extract from Antiaris toxicaria, has been reported to induce apoptosis in human gastric cancer cells. However, the mechanism and actual role of autophagy in Tox N-induced apoptosis of human gastric cancer cells remains poorly understood. In the current study, we demonstrated that Tox N could induce autophagy by inhibiting the Akt/mTOR signaling pathway in SGC-7901 cells. Moreover, we found that the inhibition of autophagy by 3-methyladenine, an autophagy inhibitor, enhanced Tox N-induced apoptotic cell death. However, the stimulation of autophagy by rapamycin, an autophagy activator, remarkably suppressed Tox N-induced apoptosis, suggesting that autophagy plays a protective role in Tox N-induced apoptosis. Thus, the results from this study suggested that Tox N combination with an autophagy inhibitor might be a promising strategy to enhance the anticancer activity of Tox N for the treatment of human gastric cancer.

Toxicarioside N induces apoptosis in human gastric cancer SGC- 7901 cell by activating the p38MAPK pathway

Huan-ge Zhao,Song-lin Zhou,Ying-ying Lin,Hao Fu Dai,Feng-Ying Huang 대한약학회 2018 Archives of Pharmacal Research Vol.41 No.1

Natural plant compounds with potent proliferationinhibition and apoptosis induction properties havebeen screened as novel anticancer drugs. Toxicarioside N(Tox N) was isolated from the seeds of the tropical plantAntiaris toxicaria in Hainan province, China. To ourknowledge, the effects that Tox N has on the apoptosis ofSGC-7901 cells and its potential mechanism have neverbeen investigated. In this study, we detected the anticanceractivities of Tox N and explored the potential mechanismin the human gastrointestinal cancer cell line SGC-7901. Here, we found that Tox N inhibited SGC-7901 cell growthin a dose- and time-dependent manner and induced apoptosisin cells based on cell morphology and flow cytometryanalyses. Additionally, the SGC-7901 cell treated with ToxN up-regulated the expression level of cleaved caspase-3/9and PARP, increased the Bax/Bcl-2 ratio, and led to therelease of cytochrome c into the cytoplasm. In addition,Tox N treatment led to the phosphorylation of p38MAPK. SB203580, a p38MAPK inhibitor, partially attenuated ToxN induced apoptosis by preventing the activation of caspase-3/9 and PARP. Our results indicated for the first timethat Tox N can induce SGC-7901 cells apoptosis by activatingthe p38MAPK pathway.

Association between PM2.5 exposure and risk of Parkinson’s disease in individuals with chronic obstructive pulmonary disease in Taiwan: a nested case-control study

Ci-Wen Luo(Ci-Wen Luo),Yu-Hsiang Kuan(Yu-Hsiang Kuan),Wen-Ying Chen(Wen-Ying Chen),Chun-Jung Chen(Chun-Jung Chen),Frank Cheau-Feng Lin(Frank Cheau-Feng Lin ),Stella Chin-Shaw Tsai(Stella Chin-Shaw Tsa 한국역학회 2023 Epidemiology and Health Vol.45 No.-

OBJECTIVES: This cohort study investigated the correlation between Parkinson’s disease (PD) risk and chronic obstructive pulmonary disease (COPD) risk under particulate matter with an aerodynamic diameter ≤2.5 μm (PM2.5) exposure. METHODS: Data from the National Health Research Institutes of Taiwan were used in this study. The Environmental Protection Administration of Taiwan established an air quality monitoring network for monitoring Taiwan’s general air quality. COPD was indicated by at least 3 outpatient records and 1 hospitalization for COPD. After the implementation of age, sex, and endpoint matching at a 1:4 ratio, 137 patients and 548 patients were included in the case group and control group, respectively. Based on the 2005 World Health Organization (WHO) standards, monthly air particle concentration data were classified into the following 4 groups in analyses of exposure–response relationships: normal level, and 1.0, 1.5, and 2.0 times the WHO level ([concentration ≥2]×25 μg/m3×number of exposure months). RESULTS: A multivariate logistic regression revealed that the 1.0 and 1.5 WHO level groups did not significantly differ from the normal level group, but the 2.0 WHO level did (odds ratio, 4.091; 95% confidence interval, 1.180 to 14.188; p=0.038). CONCLUSIONS: Elevated PM2.5 concentrations were significantly correlated with an increased risk of PD among patients with COPD. Furthermore, exposure to high PM2.5 levels can further increase the risk of PD.

Regulatory Role of SFN Gene in Hepatocellular Carcinoma and Its Mechanism

Ying Hui,Hao Zeng,Yi Feng,Wenzhou Qin,Peisheng Chen,Lifang Huang,Wenfu Zhong,Liwen Lin,Hui Lv,Xue Qin 한국생물공학회 2021 Biotechnology and Bioprocess Engineering Vol.26 No.3

Purpose: This study aims to explore the differential expression of SFN gene and its regulatory role in different hepatocarcinoma cells, and the impact on hepatocarcinoma. Materials and Methods: High and low SFN expression cells were screened by qRT-PCR and western blotting methods. SFN over expression and interference vectors were constructed. Cell viability was detected by CCK8 kit, cell cycle and apoptosis were detected by flow cytometry. Cell invasion and migration were detected. CCNB1 and CDK1 expression levels were detected by qRT-PCR and Western blotting methods. Results: The high SFN expression BEL7402 cells and the low SFN expression Hep3B cells were screened from Hep3B, HepG2, and BEL7402 cells. The activity of Hep3B cells overexpression vector SFNpcDNA3.1(+) decreased and apoptosis increased, the ratio of G0/G1 decreased and the ratio of S phase increased. The activity of BEL7402 cells transfected with SFN siRNA decreased and apoptosis increased, the ratio of G0/G1 decreased and the ratio of G2/M increased. Interference and overexpression vectors have little effect on the invasion and migration of the two cells. The expression of CDK1 in Hep3B cells decreased significantly, the expression of CDK1 and CCNB1 in BEL7402 cells increased significantly. Conclusions: The differentially expressed SFN gene can regulate the growth of the two hepatocarcinoma cells, high expression of SFN gene can inhibit their growth. The mechanism may be achieved by regulating CCNB1 and CDK1 expression.

Unilateral ureteral obstruction causes gut microbial dysbiosis and metabolome disorders contributing to tubulointerstitial fibrosis

Lin Chen,Dan-Qian Chen,Jing-Ru Liu,Jun Zhang,Nosratola D. Vaziri,Shougang Zhuang,Hua Chen,Ya-Long Feng,Yan Guo,Ying-Yong Zhao 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-

Chronic kidney disease (CKD) increases the risk and prevalence of cardiovascular disease (CVD) morbidity and mortality. Recent studies have revealed marked changes in the composition of the microbiome and the metabolome and their potential influence in renal disease and CVD via the accumulation of microbial-derived uremic toxins. However, the effect of unilateral ureteral obstruction (UUO) on the gut microbiome and circulating metabolites is unknown. Male Sprague-Dawley rats were randomized to UUO and sham-operated control groups. Renal histology, colonic microbiota, and plasma metabolites were examined two weeks later. We employed 16S rRNA sequence and untargeted metabolomic analyses to explore the changes in colonic microbiota and plasma metabolites and their relationship with tubulointerstitial fibrosis (TIF). The UUO rats exhibited tubular atrophy and dilatation, interstitial fibrosis and inflammatory cell infiltration in the obstructed kidney. UUO rats showed significant colonic enrichment and depletion of genera. Significant differences were identified in 219 plasma metabolites involved in lipid, amino acid, and bile acid metabolism, which were consistent with gut microbiota-related metabolism. Interestingly, tryptophan and its metabolites kynurenine, 5-hydroxytryptophan and 5-hydroxytryptamine levels, which were linked with TIF, correlated with nine specific genera. Plasma tryptophan level was positively correlated with Clostridium IV, Turicibacter, Pseudomonas and Lactobacillales, and negatively correlated with Oscillibacter, Blautia, and Intestinimonas, which possess the genes encoding tryptophan synthase (K16187), indoleamine 2,3-dioxygenase (K00463) and tryptophan 2,3-dioxygenase (K00453) and their corresponding enzymes (EC:1.13.11.52 and EC:1.13.11.11) that exacerbate TIF. In conclusion, UUO results in profound changes in the gut microbiome and circulating metabolites, events that contribute to the pathogenesis of inflammation and TIF.

외국문헌초록(外國文獻草綠) : UASB와 MBR의 결합에서 손쉬운 질산화, 탈질화 및 메탄형성의 통합

Ying Yu An,Feng Lin Yang,Hwee Chuan Chua,Fook Sin Wong,Bing Wu 한국수처리학회 2009 한국수처리학회지 Vol.17 No.2

Quality of Life for Patients with Esophageal/Gastric Cardia Precursor Lesions or Cancer: A One-year Prospective Study

Wen, Ying,Pan, Xiong-Fei,Huang, Wen-Zhi,Zhao, Zhi-Mei,Wei, Wen-Qiang,Chen, Feng,Lan, Hui,Huang, He,Yang, Chun-Xia,Qiao, You-Lin Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.1

Background: The current study examined health-related quality of life (QoL) for patients with esophageal/gastric cardia precursor lesions or cancer before and after treatment to facilitate improved prevention and treatment. Materials and Methods: Patients with different stages of esophageal/gastric cardia lesions completed two QoL questionnaires, EORTC QLQ-C30 and supplemental QLQ-OES 18, before primary treatment, and at 1, 6 and 12 months after treatment. Results: Fifty-nine patients with precursor lesions, 57 with early stage cancer, and 43 with advanced cancer responded to our survey. Patients with precursor lesions or early stage cancer reported better QoL overall than those with advanced cancer before treatment (p<0.01). Global QoL scores before treatment and at 1 month after treatment were $71{\pm}9$ versus $69{\pm}9$ (p>0.01), $71{\pm}8$ versus $61{\pm}11$ (p<0.01), $67{\pm}11$ versus $62{\pm}9$ (p<0.01) for three stages of lesions. At 6 months after treatment, some QoL measures recovered gradually in precursor lesion and early cancer patients, while some continuously deteriorated in advanced cancer patients. At 12 months, all QoL scores were comparable to baseline for patients with precursor lesions (p>0.01), while global QoL, social, pain, and insomnia scores for early stage and advanced cancer were inferior to corresponding baseline levels (difference between means>5, p<0.01). At this time point, compared with patients with early stage cancer, those with advanced cancer showed worse QoL with all function and most symptom measures (p<0.01). Conclusions: Patients with precursor lesions or early stage esophageal/gastric cardia cancer show better QoL than those with advanced cancer. This indicates that screening, early diagnosis and treatment may improve the QoL for esophageal/gastric cardia cancer patients. Target intervention and counseling should be given by health care providers during treatment and follow-up to facilitate QoL improvement.

Graphite-based selectorless RRAM: improvable intrinsic nonlinearity for array applications

Chen, Ying-Chen,Hu, Szu-Tung,Lin, Chih-Yang,Fowler, Burt,Huang, Hui-Chun,Lin, Chao-Cheng,Kim, Sungjun,Chang, Yao-Feng,Lee, Jack C. The Royal Society of Chemistry 2018 Nanoscale Vol.10 No.33

<P>Selectorless graphite-based resistive random-access memory (RRAM) has been demonstrated by utilizing the intrinsic nonlinear resistive switching (RS) characteristics, without an additional selector or transistor for low-power RRAM array application. The low effective dielectric constant value (<I>k</I>) layer of graphite or graphite oxide is utilized, which is beneficial in suppressing sneak-path currents in the crossbar RRAM array. The tail-bits with low nonlinearity can be manipulated by the positive voltage pulse, which in turn can alleviate variability and reliability issues. Our results provide additional insights for built-in nonlinearity in 1<I>R</I>-only selectorless RRAMs, which are applicable to the low-power memory array, ultrahigh density storage, and in-memory neuromorphic computational configurations.</P>