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39 results on '"Fan, Jinshuo"'

7. Construction and validation of a nomogram based on N6‐Methylandenosine‐related lncRNAs for predicting the prognosis of non‐small cell lung cancer patients.

Author

Xiao, Wenjing, Geng, Wei, Xu, Juanjuan, Huang, Qi, Fan, Jinshuo, Tan, Qi, Yin, Zhengrong, Li, Yumei, Yang, Guanghai, and Jin, Yang

Subjects
NON-small-cell lung carcinoma, CANCER patients, TUMOR-infiltrating immune cells, LINCRNA, NOMOGRAPHY (Mathematics)
Abstract

Background: The N6‐methyladenosine (m6A) can modify long non‐coding RNAs (lncRNAs), thereby influencing a wide array of biological functions. However, the prognosis of m6A‐related lncRNAs (m6ARLncRNAs) in non‐small cell lung cancer (NSCLC) remains largely unknown. Methods: Pearson correlation analysis was used to identify m6ARLncRNAs in 1835 NSCLC patients and with the condition (|Pearson R| > 0.4 and p < 0.001). Univariant Cox regression analysis was conducted to explore the prognostic m6ARLncRNAs. We filtered prognostic m6ARLncRNAs by LASSO regression and multivariate Cox proportional hazard regression to construct and validate an m6ARLncRNAs signature (m6ARLncSig). We analyzed the correlation between the m6ARLncSig score and clinical features, immune microenvironment, tumor mutation burden, and therapeutic sensitivity and conducted independence and clinical stratification analysis. Finally, we established and validated a nomogram for prognosis prediction in NSCLC patients. Results: Forty‐one m6ARLncRNAs were identified as prognostic lncRNAs, and 12 m6ARLncRNAs were selected to construct m6ARLncSig in the TCGA training dataset. The m6ARLncSig was further validated in the testing dataset, GSE31210, GSE37745, GSE30219, and our NSCLC samples. In terms of m6ARLncSig, NSCLC patients were divided into high‐ and low‐risk groups, with significantly different overall survival (OS), clinical features (age, sex, and tumor stage), tumor‐infiltrating immune cells, chemotherapeutic sensitivity, radiotherapeutic response, and biological pathways. Moreover, m6ARLncSig independently predicted the OS of NSCLC patients. Finally, the robustness and clinical practicability for predicting NSCLC patient prognosis was improved by constructing a nomogram containing the m6ARLncSig, age, gender, and tumor stage. Conclusions: Our study demonstrated that m6ARLncSig could act as a potential biomarker for evaluating the prognosis and therapeutic efficacy in NSCLC patients. [ABSTRACT FROM AUTHOR]

Published
2023
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18. Transmission of 2019-nCoV to Health-Care Workers in the Early Epidemic

Author

Wu, Feng, primary, Guo, Mengfei, additional, Zhang, Shuai, additional, Ma, Yanling, additional, Ma, Pei, additional, Duan, Limin, additional, Wang, Xuan, additional, Lv, Zhilei, additional, Xu, Juanjuan, additional, Fan, Jinshuo, additional, Ma, Guanzhou, additional, Yi, Jianhua, additional, Hu, Yu, additional, and Jin, Yang, additional

Published
2020
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21. The role of adrenergic receptors in lung cancer

Author

Huang, Qi, Tan, Qi, Mao, Kaimin, Yang, Guanghai, Ma, Guangzhou, Luo, Ping, Wang, Sufei, Mei, Peiyuan, Wu, Feng, Xu, Juanjuan, Guo, Mengfei, LV, Zhilei, Fan, Jinshuo, Zhang, Shuai, Wang, Xuan, and Jin, Yang

Subjects
Review Article, respiratory system, respiratory tract diseases
Abstract

Adrenergic receptors (ARs), especially β-ARs, are constitutively expressed in most mammalian cells and are associated with various malignancies including lung cancer. Epidemiologic studies have reported that activation of β-AR signalling promotes the development and progression of lung cancer and that pharmacological interference by β-AR blockers could partially reverse lung cancer progression. In this review, we mainly focus on the role of β-ARs in lung cancer and then reveal the possible application of AR blockers in anti-tumour therapy for lung cancer.

Published
2018

23. Autologous tumor cell–derived microparticle-based targeted chemotherapy in lung cancer patients with malignant pleural effusion

Author

Guo, Mengfei, primary, Wu, Feng, additional, Hu, Guorong, additional, Chen, Lian, additional, Xu, Juanjuan, additional, Xu, Pingwei, additional, Wang, Xuan, additional, Li, Yumei, additional, Liu, Shuqing, additional, Zhang, Shuai, additional, Huang, Qi, additional, Fan, Jinshuo, additional, Lv, Zhilei, additional, Zhou, Mei, additional, Duan, Limin, additional, Liao, Tingting, additional, Yang, Guanghai, additional, Tang, Ke, additional, Liu, Bifeng, additional, Liao, Xiaofei, additional, Tao, Xiaonan, additional, and Jin, Yang, additional

Published
2019
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27. Value of 18F–FDG PET/CT for predicting EGFR mutations and positive ALK expression in patients with non-small cell lung cancer: a retrospective analysis of 849 Chinese patients

Author

Lv, Zhilei, primary, Fan, Jinshuo, additional, Xu, Juanjuan, additional, Wu, Feng, additional, Huang, Qi, additional, Guo, Mengfei, additional, Liao, Tingting, additional, Liu, Shuqing, additional, Lan, Xiaoli, additional, Liao, Shanshan, additional, Geng, Wei, additional, and Jin, Yang, additional

Published
2017
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28. IL-17 induces EMT via Stat3 in lung adenocarcinoma

Author

Huang, Qi, Han, Jieli, Fan, Jinshuo, Duan, Limin, Guo, Mengfei, Lv, Zhilei, Hu, Guorong, Chen, Lian, Wu, Feng, Tao, Xiaonan, Xu, Juanjuan, and Jin, Yang

Subjects
Original Article, respiratory system, respiratory tract diseases
Abstract

Epithelial-mesenchymal transition (EMT) plays a vital role in lung inflammatory diseases, including lung cancer. However, the role and mechanism of action of the proinflammatory cytokine IL-17 in EMT in lung adenocarcinoma remain unresolved. In our study, we discovered that the expression of N-cadherin, Vimentin, Snail1, Snail2, and Twist1 was positively correlated with IL-17 expression, while E-cadherin expression was negatively correlated with IL-17 expression in human lung adenocarcinoma tissues. Moreover, we confirmed that IL-17 promoted EMT in A549 and Lewis lung carcinoma (LLC) cells in vitro by upregulating N-cadherin, Vimentin, Snail1, Snail2, and Twist1 expression and downregulating E-cadherin expression. Stat3 was activated in IL-17-treated A549 and LLC cells, and Stat3 inhibition or siRNA knockdown notably reduced IL-17-induced EMT in A549 and LLC cells. Thus, IL-17 promotes EMT in lung adenocarcinoma via Stat3 signaling; these observations suggest that targeting IL-17 and EMT are potential novel therapeutic strategies for lung cancer.

Published
2016

29. The Role of Interleukin-17 in Lung Cancer

Author

Wu, Feng, Xu, Juanjuan, Huang, Qi, Han, Jieli, Duan, Limin, Fan, Jinshuo, Lv, Zhilei, Guo, Mengfei, Hu, Guorong, Chen, Lian, Zhang, Shuai, Tao, Xiaonan, Ma, Wanli, and Jin, Yang

Subjects
Article Subject
Abstract

Tumour-associated inflammation is a hallmark of malignant carcinomas, and lung cancer is a typical inflammation-associated carcinoma. Interleukin-17 (IL-17) is an important inflammatory cytokine that plays an important role in chronic inflammatory and autoimmune diseases and in inflammation-associated tumours. Numerous studies have shown that IL-17 directly or indirectly promotes tumour angiogenesis and cell proliferation and that it inhibits apoptosis via the activation of inflammatory signalling pathways. Therefore, IL-17 contributes to the metastasis and progression of lung cancer. Research advances with respect to the role of IL-17 in lung cancer will be presented as a review in this paper.

Published
2016
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30. The ACE2/Angiotensin-(1–7)/Mas Receptor Axis: Pleiotropic Roles in Cancer

Author

Xu, Juanjuan, primary, Fan, Jinshuo, additional, Wu, Feng, additional, Huang, Qi, additional, Guo, Mengfei, additional, Lv, Zhilei, additional, Han, Jieli, additional, Duan, Limin, additional, Hu, Guorong, additional, Chen, Lian, additional, Liao, Tingting, additional, Ma, Wanli, additional, Tao, Xiaonan, additional, and Jin, Yang, additional

Published
2017
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37. The role of adrenergic receptors in lung cancer.

Author

Huang Q, Tan Q, Mao K, Yang G, Ma G, Luo P, Wang S, Mei P, Wu F, Xu J, Guo M, Lv Z, Fan J, Zhang S, Wang X, and Jin Y

Abstract

Adrenergic receptors (ARs), especially β-ARs, are constitutively expressed in most mammalian cells and are associated with various malignancies including lung cancer. Epidemiologic studies have reported that activation of β-AR signalling promotes the development and progression of lung cancer and that pharmacological interference by β-AR blockers could partially reverse lung cancer progression. In this review, we mainly focus on the role of β-ARs in lung cancer and then reveal the possible application of AR blockers in anti-tumour therapy for lung cancer., Competing Interests: None.

Published
2018

38. Integrative genomic analysis of interleukin-36RN and its prognostic value in cancer.

Author

Lv Z, Fan J, Zhang X, Huang Q, Han J, Wu F, Hu G, Guo M, and Jin Y

Subjects
Amino Acid Sequence, Animals, Computer Simulation, Conserved Sequence genetics, Databases, Genetic, Exons genetics, Gene Expression Profiling, Gene Expression Regulation, Genome, Humans, Interleukins chemistry, Introns genetics, Molecular Sequence Data, Mutation genetics, Oligonucleotide Array Sequence Analysis, Phylogeny, Polymorphism, Single Nucleotide genetics, Prognosis, Proteomics, Sequence Alignment, Vertebrates genetics, Genomics methods, Interleukins genetics, Neoplasms genetics
Abstract

Interleukin (IL)-36RN, previously known as IL1-F5 and IL-1δ, shares a 360-kb region of chromosome 2q13 with members of IL-1 systems. IL-36RN encodes an anti-inflammatory cytokine, IL-36 receptor antagonist (IL-36Ra). In spite of IL-36Ra showing the highest homology to IL-1 receptor (IL-1R) antagonist, it differs from the latter in aspects including its binding to IL-lRrp2 but not to IL-1R1. IL-36RN is mainly expressed in epithelial cells and has important roles in inflammatory diseases. In the present study, IL-36RN was identified in the genomes of 27 species, including human, chimpanzee, mouse, horse and dolphin. Human IL-36RN was mainly expressed in the eye, head and neck, fetal heart, lung, testis, cervix and placenta; furthermore, it was highly expressed in bladder and parathyroid tumors. Furthermore, a total of 30 single nucleotide polymorphisms causing missense mutations were determined, which are considered to be the causes of various diseases, such as generalized pustular psoriasis. In addition, the link between IL-36RN and the prognosis of certain cancer types was revealed through meta-analysis. Tumor-associated transcriptional factors c-Fos, activator protein-1, c-Jun and nuclear factor κB were found to bind to the upstream region in the IL-36RN gene. This may indicate that IL-36RN is involved in tumorigenesis and tumor progression through the regulation of tumor-associated transcriptional factors. The present study identified IL-36RN in various species and investigated the associations between IL-36RN and cancer prognosis, which would determine whether IL-36RN drove the evolution of the various species with regard to tumorigenesis.

Published
2016
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39. IL-17 induces EMT via Stat3 in lung adenocarcinoma.

Author

Huang Q, Han J, Fan J, Duan L, Guo M, Lv Z, Hu G, Chen L, Wu F, Tao X, Xu J, and Jin Y

Abstract

Epithelial-mesenchymal transition (EMT) plays a vital role in lung inflammatory diseases, including lung cancer. However, the role and mechanism of action of the proinflammatory cytokine IL-17 in EMT in lung adenocarcinoma remain unresolved. In our study, we discovered that the expression of N-cadherin, Vimentin, Snail1, Snail2, and Twist1 was positively correlated with IL-17 expression, while E-cadherin expression was negatively correlated with IL-17 expression in human lung adenocarcinoma tissues. Moreover, we confirmed that IL-17 promoted EMT in A549 and Lewis lung carcinoma (LLC) cells in vitro by upregulating N-cadherin, Vimentin, Snail1, Snail2, and Twist1 expression and downregulating E-cadherin expression. Stat3 was activated in IL-17-treated A549 and LLC cells, and Stat3 inhibition or siRNA knockdown notably reduced IL-17-induced EMT in A549 and LLC cells. Thus, IL-17 promotes EMT in lung adenocarcinoma via Stat3 signaling; these observations suggest that targeting IL-17 and EMT are potential novel therapeutic strategies for lung cancer.

Published
2016

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