Yu Sun

Xiangya Hospital Central South University

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Zhanyu Xu

First Affiliated Hospital of GuangXi Medical University

Jiangbo Wei

National Natural Science Foundation of China

Fanglu Qin

Guangxi Medical University

Shikang Li

First Affiliated Hospital of GuangXi Medical University

Liqiang Yuan

Deyang Stomatological Hospital

Sheng-Hua Lin

National Natural Science Foundation of China

Xiangsen Liang

Guangxi Medical University

Shengzhuang Yang

Guangxi Medical University

Tao Liu

Northwest A&F University

Wenzhou Liu

Sun Yat-sen Memorial Hospital

Cooperative Institutions

Guangxi Medical University

First Affiliated Hospital of GuangXi Medical University

Huazhong University of Science and Technology

Jilin University

Central South University

First Hospital of Jilin University

Sun Yat-sen University

Sichuan University

Capital Medical University

Shanghai Jiao Tong University

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Clinical significance and potential molecular mechanism of miRNA-222-3p in metastatic prostate cancer

Bioengineered (2020)

Yu Sun Gang Chen Juan He Zhi‐Guang Huang Shenghua Li

The clinical significance and underlying molecular mechanism of miRNA-222-3p in metastatic prostate cancer (MPCa) remain unclear. The present study used a large number of cases (n = 1,502) based on miRNA chip and miRNA sequencing datasets to evaluate the expression and diagnostic potential of miRNA-222-3p in MPCa. We applied a variety of meta-analytic methods, including forest maps, sensitivity analysis, subgroup analysis and summary receiver operating characteristic curves, to prove the final results. MiRNA-222-3p was reduced in MPCa and had a moderate diagnostic potential in MPCa. We screened 118 miRNA-222-3p targets using three different methods including miRNA-222-3p transfected MPCa cell lines, online prediction databases and differently upregulated genes in MPCa. Moreover, functional enrichment analysis performed to explore the potential molecular mechanism of miRNA-222-3p showed that the potential target genes of miRNA-222-3p were significantly enriched in the p53 signal pathway. In the protein–protein interaction network analysis, SNAP91 was identified as a hub gene that may be closely related to MPCa. Gene chip and RNA sequencing datasets containing 1,237 samples were used to determine the expression level and diagnostic potential of SNAP91 in MPCa. SNAP91 was found to be overexpressed in MPCa and had a moderate diagnostic potential in MPCa. In addition, miRNA-222-3p expression was negatively correlated with SNAP91 expression in MPCa (r = −0.636, P = 0.006). These results demonstrated that miRNA-222-3p might play an important role in MPCa by negatively regulating SNAP91 expression. Thus, miRNA-222-3p might be a potential biomarker and therapeutic target of MPCa.

10.1080/21655979.2020.1867405

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Clinical Significance and Underlying Mechanisms of CELSR3 in Metastatic Prostate Cancer Based on Immunohistochemistry, Data Mining, andIn SilicoAnalysis

Cancer Biotherapy and Radiopharmaceuticals (2021)

Yu Sun Gang Chen Juan He Jing-Xiao Li Xiang-Yu Gan

Background: The treatment and survival rate of patients with metastatic prostate cancer (MPCa) remain unsatisfactory. Herein, the authors investigated the clinical value and potential mechanisms of cadherin EGF LAG seven-pass G-type receptor 3 (CELSR3) in MPCa to identify novel targets for clinical diagnosis and treatment. Materials and Methods: mRNA microarray and RNA-Seq (n = 1246 samples) data were utilized to estimate CELSR3 expression and to assess its differentiation ability in MPCa. Similar analyses were performed with miRNA-221-3p. Immunohistochemistry performed on clinical samples were used to evaluate the protein expression level of CELSR3 in MPCa. Based on CELSR3 differentially coexpressed genes (DCEGs), enrichment analysis was performed to investigate potential mechanisms of CELSR3 in MPCa. Results: The pooled standard mean difference (SMD) for CELSR3 was 0.80, demonstrating that CELSR3 expression was higher in MPCa than in localized prostate cancer (LPCa). CELSR3 showed moderate potential to distinguish MPCa from LPCa. CELSR3 protein expression was found to be markedly upregulated in MPCa than in LPCa tissues. The authors screened 894 CELSR3 DCEGs, which were notably enriched in the focal adhesion pathway. miRNA-221-3p showed a significantly negative correlation with CELSR3 in MPCa. Besides, miRNA-221-3p expression was downregulated in MPCa than in LPCa (SMD = −1.04), and miRNA-221-3p was moderately capable of distinguishing MPCa from LPCa. Conclusions: CELSR3 seems to play a pivotal role in MPCa by affecting the focal adhesion pathway and/or being targeted by miRNA-221-3p.

10.1089/cbr.2021.0178

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Downregulation of miRNA-205 Expression and Biological Mechanism in Prostate Cancer Tumorigenesis and Bone Metastasis

BioMed Research International (2020)

Yu Sun Shenghua Li Jiwen Cheng Gang Chen Zhi‐Guang Huang

The expression and mechanism of microRNA-205 (miRNA-205) in prostate cancer (PCa) and its bone metastasis remain controversial.The expression and discriminating capability of miRNA-205 were assessed by drawing a forest plot and a summarized receiver operating characteristic (SROC) curve, using data available from 27 miRNA-array and miRNA-sequencing datasets. The miRNA-205 target genes were acquired from online prediction tools, differentially upregulated genes in PCa, and differentially expressed genes (DEGs) after miRNA-205 transfection into PCa cell lines. Functional enrichment analysis was conducted to explore the biological mechanism of miRNA-205 targets. Immunohistochemistry (IHC) was applied to verify the protein level of the hub gene.The expression of miRNA-205 in the PCa group (1,461 samples) was significantly lower than that in the noncancer group (510 samples), and the downregulation of miRNA-205 showed excellent sensitivity and specificity in differentiating between the two groups. In bone metastatic PCa, the miRNA-205 level was further reduced than in nonbone metastatic PCa, and it showed a good capability in distinguishing between the two groups. In total, 153 miRNA-205 targets were screened through the three aforementioned methods. Based on the results of functional enrichment analysis, the targets of miRNA-205 were mainly enriched during chromosome segregation and phospholipid-translocating ATPase activity and in the spindle microtubule and the p53 signaling pathway. CDK1 had the highest connectivity in the PPI network analysis and was screened as one of the hub genes. A statistically significant negative correlation between miRNA-205 and CDK1 was observed. The expression of CDK1 in PCa samples was pronouncedly upregulated in terms of both the mRNA level and the protein level when compared with noncancer samples.miRNA-205 may play a vital role in PCa tumorigenesis and bone metastasis by targeting CDK1.

10.1155/2020/6037434

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The long noncoding RNA LINC00483 promotes lung adenocarcinoma progression by sponging miR-204-3p

Cellular & Molecular Biology Letters (2019)

Shengzhuang Yang Tao Liu Yu Sun Xiangsen Liang

Abstract Background The expression of the long noncoding RNA LINC00483 is upregulated in lung adenocarcinoma (LUAD). However, its role in the progression of LUAD and the underlying mechanisms remain elusive. Methods The expressions of LINC00483 and miR-204-3p were determined using quantitative real-time PCR. The correlation between the clinicopathological characteristics of LUAD patients and LINC00483 expression was analyzed using Pearson’s χ 2 test. A549 and PC-9 cells were transfected with small interfering RNA (siRNA) that specially targeting LINC00483 to assess the impact of its knockdown. Cell proliferation was assessed using the Cell Counting Kit-8 and clone forming assays. Cell migration and cell invasion were evaluated using a transwell assay. The levels of Snail, E-cadherin, N-cadherin and ETS1 proteins were determined via western blotting. The interaction between LINC00483 and miR-204-3p was analyzed using dual-luciferase, fluorescence in situ hybridization and RNA immunoprecipitation. Results LINC00483 was upregulated in LUAD tissues and cell lines. Higher LINC00483 levels closely correlated to shorter survival times, advanced TNM stage, larger tumor size and positive lymph node metastasis. Cell proliferation, migration and invasion were suppressed after LINC00483 knockdown. LINC00483 mainly localized in the cytoplasm, where it acted as a sponge of miR-204-3p. ETS1 was validated as a downstream target of miR-204-3p and is thus regulated by LINC00483. Conclusion This study demonstrated that LINC00483 facilitates the proliferation, migration and invasion of LUAD cells by acting as a sponge for miR-204-3p, which in turn regulates ETS1.

Tumor progression

clone (Java method)

10.1186/s11658-019-0192-7

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Breath control strategies for English coherent pronunciation based on the biomechanics of respiratory muscles

Molecular & cellular biomechanics (2025)

W. Xu Ting Luan Ying Zhang Yu Sun

This paper aims to solve the problem of insufficient breath and lack of coordination between breathing and pronunciation in English learners’ coherent pronunciation. By analyzing the biomechanical characteristics of respiratory muscles, scientific breath control strategies are designed to optimize airflow management and improve speech fluency and expression efficiency. English learners of different language levels were recruited and divided into elementary, intermediate and advanced groups. Speech tasks including slow pronunciation, fast pronunciation and long sentence pronunciation were designed. Electromyography was used to record the activity characteristics of respiratory muscles, airflow meter was used to measure airflow output data, and high-sensitivity microphone combined with Praat software was used to extract speech features including speaking rate and pause frequency. This paper studies tasks such as slow pronunciation, fast pronunciation and long sentence pronunciation, clarifies the degree of involvement of key muscles such as the diaphragm, and designs targeted phased breath control strategies, including abdominal breathing training, long sentence reading and coherent reading simulation, and the introduction of speech tasks. The results show that the breath control strategy proposed in this paper significantly improves learners’ speech fluency, syllable and phonetic pronunciation accuracy under all task conditions. At a speaking speed of 180 words/minute, the correct pronunciation rate of phonetic symbols and syllables in this strategy intervention was 80%, and the correct pronunciation rate of syllables was 83%, and the breath maintenance rate and pause frequency were improved. The optimization strategy based on respiratory biomechanics can effectively improve language learners’ breath management ability and coherent pronunciation level, and provide an innovative theoretical basis and practical path for language learning and voice training.

Biomechanics

Pronunciation

10.62617/mcb998

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[Bioinformatic screening of key genes controlling the development and progression of lung cancer].

DOAJ (DOAJ: Directory of Open Access Journals) (2012)

Junlong Wang Jun‐Jie Shi Wenzhou Liu Yu Sun Hua‐Fu Zhou

Lung cancer is the most common cancer in the world. The gene expression profiling of lung cancer has been extensively investigated. However, only a few studies have identified the possible pathways and significant genes related to lung cancer. The aim of this study is to explore the large number of lung cancer-related microarray datasets and identify the crucial genes that can benefit the understanding of the progression and development of this disease.To identify the genes that effected lung cancer at the mRNA level, gene set enrichment analysis was used to analyze six selected gene expression datasets.Among the six gene expression datasets, 3 up-regulated and 26 down-regulated pathways were found by gene set enrichment analysis. We found 11 significant genes with P < 0.05 from the results of tight junction meta-analysis of the six data sets.The tight junction pathway plays an important role in the study of the occurrence and development of lung cancer. Significant genes within the pathways will be further discussed in future studies.

10.3779/j.issn.1009-3419.2012.11.07

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Rapamycin suppresses the PI3K/AKT/mTOR signaling pathway by targeting SIRT1 in esophageal cancer

Experimental and Therapeutic Medicine (2021)

Tao Liu Xiangsen Liang Yu Sun Shengzhuang Yang

Rapamycin, a secondary metabolite produced by Streptomyces hygroscopicus, is known for its pharmacological effects, especially antitumor and immunosuppressive activities. However, the antitumoral effects of rapamycin in human esophageal cancer (EC) are still poorly understood. To investigate the potential of rapamycin in EC treatment, sirtuin 1 (SIRT1) mRNA expression was quantified in the tissue of patients with EC or in EC cell lines using reverse transcription‑quantitative PCR. The protein levels of SIRT1 and PI3K/AKT/mTOR were measured via western blotting. Furthermore, cell viability, migration and invasion were investigated by Cell Counting Kit‑8, wound healing and Transwell assays, respectively. The present results suggested that SIRT1 expression was upregulated in EC. In vitro, the inhibitory effect of rapamycin on cell viability in EC was strengthened or weakened after small interfering (si)‑SIRT1 or pcDNA3.1/SIRT1 transfection. Furthermore, SIRT1 rescued the inhibitory effect of rapamycin on the migration and invasion of EC cells. In vivo, si‑SIRT1 or SIRT1 overexpression in mice could enhance or rescue the inhibitory effects of rapamycin on tumor growth. In addition, SIRT1 transfection rescued the decreased level of phosphorylated (p)‑PI3K, p‑AKT and p‑mTOR induced by rapamycin treatment. Taken together, the present results suggested that rapamycin suppressed the cell viability, migration, invasion and PI3K/AKT/mTOR signaling pathway in EC by negatively regulating SIRT1.

Viability assay

RPTOR

Sirtuin 1

10.3892/etm.2021.10624

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<p>B3GNT3, a Direct Target of miR-149-5p, Promotes Lung Cancer Development and Indicates Poor Prognosis of Lung Cancer</p>

Cancer Management and Research (2020)

Yu Sun Tao Liu Lei Xian Wenzhou Liu Jun Liu

B3GNT3 (β1, 3-N-acetylglucosaminyltransferase-3) belongs to the β3GlcNAcT family and is essential to form extended core 1 oligosaccharides. Previous studies revealed that B3GNT3 expression was dysregulated in multiple cancers. Here, we aimed to understand the expression profile and function of B3GNT3 in lung cancer.The expression of B3GNT3 was measured by immunohistochemistry and public database analysis. B3GNT3 was knocked down to evaluate the lung cancer cell proliferation, migration and invasion in in vitro and in vivo tumor formation experiments. miR-149-5p targeting B3GNT3 was identified with TargetScan analysis and confirmed with reporter assay. Overexpression of miR-149-5p was achieved using microRNA mimics and function of microRNA-149-5p/B3GNT3 axis was tested in vitro.B3GNT3 was upregulated in lung cancer, and B3GNT3 overexpression was associated with poor prognosis of lung cancer patients. High expression of B3GNT3 was associated with advanced TNM stages, larger tumor size, tumor metastasis and recurrence. Functionally, we demonstrated that knockdown of B3GNT3 suppressed lung cancer cell growth and invasion in vitro. Knockdown of B3GNT3 suppressed lung cancer development in a xenograft tumor model. Moreover, miR-149-5p was validated to negatively regulate B3GNT3 expression through directly targeting B3GNT3 3'-UTR. Overexpression of miR-149-5p could antagonize the tumorigenesis effect of B3GNT3 in vitro.In summary, our study demonstrated that B3GNT3 overexpression was correlated with poor prognosis of lung cancer patient, indicating that B3GNT3 could be a promising prognostic biomarker for lung cancer. miR-149-5p negatively regulated B3GNT3 expression, which might be utilized for therapeutic target in lung cancer.

10.2147/cmar.s236565

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Acinetobacter nosocomialis utilizes a unique type VI secretion system to promote its survival in niches with prey bacteria

mBio (2024)

Yu Sun Lidong Wang Ming Zhang Jing Jie Qingtian Guan

Pathogenic bacteria of the

Acinetobacter baumannii

10.1128/mbio.01468-24

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Clinical Significance And Potential Mechanisms of The RNA Methyltransferase KIAA1429 In Osteosarcoma

Research Square (Research Square) (2021)

Yu Sun Yiwu Lei Shu-Fan Ji Hao Wu Yun Liu

Abstract Background: KIAA1429, a member of the RNA methyltransferase complex, is involved in cancer progression. However, the clinical significance of KIAA1429 in osteosarcoma (OS) and the underlying mechanisms by which it contributes to disease progression remain unclear. Methods: The clinical significance of KIAA1429 in OS was evaluated based on the RT-qPCR, microarray, RNA sequencing, and published data. Two lentivirus-mediated KIAA1429-targeting siRNA constructs were transfected into SW1353 cells, and CCK-8 and flow cytometry assays were applied to investigate the biological function of KIAA1429 in OS cells. KIAA1429-related genes in OS were identified from lists of co-expressed genes (CEGs) and differentially expressed genes (DEGs). Functional enrichment analysis was employed to explore the potential mechanisms by which KIAA1429 contributes to the progression of OS. Results: The mRNA expression of KIAA1429 was notably overexpressed in 250 OS samples than 71 non-cancer samples (SMD=0.74). SROC curve analysis showed that KIAA1429 exhibits diagnostic capacity between OS samples and non-cancer samples (AUC=0.83). Survival analysis showed that overexpression of KIAA1429 was associated with shorter overall survival time. Knocking down KIAA1429 reduced the level of m6A methylation, inhibited proliferation, and accelerated apoptosis in OS cells. A total of 395 KIAA1429-related genes were identified, and were enriched in the cell cycle pathway. Protein–protein interaction (PPI) network analysis showed that CDK1, CCNA2, and CCNB1 were KIAA1429-related genes that act as major network hubs in OS. Conclusion: KIAA1429 plays an oncogenic role in OS and may facilitate the progression of OS through a mechanism involving the regulation of CDK1, CCNA2, and CCNB1.

Tumor progression

10.21203/rs.3.rs-227839/v2

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