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Pancreatic Neoplasms: HELP
Articles by J. Liu
Based on 7 articles published since 2010
(Why 7 articles?)
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Between 2010 and 2020, J. Liu wrote the following 7 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article [Prognostic value of tumor infiltration immune cells in pancreatic cancer]. 2018

Zhao, K L / Liu, J / Jiang, W N / Hao, J H. ·Department of Pancreatic Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China. ·Zhonghua Wai Ke Za Zhi · Pubmed #29886672.

ABSTRACT:

2 Article Delineating the Role of βIV-Tubulins in Pancreatic Cancer: βIVb-Tubulin Inhibition Sensitizes Pancreatic Cancer Cells to Vinca Alkaloids. 2016

Sharbeen, G / McCarroll, J / Liu, J / Youkhana, J / Limbri, L F / Biankin, A V / Johns, A / Kavallaris, M / Goldstein, D / Phillips, P A. ·Pancreatic Cancer Translational Research Group, Lowy Cancer Research Centre, Prince of Wales Clinical School, University of New South Wales (UNSW), Sydney, Australia, 2052. · Children's Cancer Institute, Lowy Cancer Research Centre, UNSW, Sydney, Australia, 2031; Australian Centre for NanoMedicine, ARC Centre of Excellence in Convergent Bio-Nano Science and Technology, UNSW, Australia. · The Kinghorn Cancer Centre, Cancer Program, Garvan Institute of Medical Research, Darlinghurst, Sydney, Australia; Wolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Bearsden, Glasgow, Scotland G61 1BD, United Kingdom. · The Kinghorn Cancer Centre, Cancer Program, Garvan Institute of Medical Research, Darlinghurst, Sydney, Australia. · Pancreatic Cancer Translational Research Group, Lowy Cancer Research Centre, Prince of Wales Clinical School, University of New South Wales (UNSW), Sydney, Australia, 2052; Australian Centre for NanoMedicine, ARC Centre of Excellence in Convergent Bio-Nano Science and Technology, UNSW, Australia. Electronic address: p.phillips@unsw.edu.au. ·Neoplasia · Pubmed #27889644.

ABSTRACT: Pancreatic cancer (PC) is a lethal disease which is characterized by chemoresistance. Components of the cell cytoskeleton are therapeutic targets in cancer. βIV-tubulin is one such component that has two isotypes-βIVa and βIVb. βIVa and βIVb isotypes only differ in two amino acids at their C-terminus. Studies have implicated βIVa-tubulin or βIVb-tubulin expression with chemoresistance in prostate, breast, ovarian and lung cancer. However, no studies have examined the role of βIV-tubulin in PC or attempted to identify isotype specific roles in regulating cancer cell growth and chemosensitivity. We aimed to determine the role of βIVa- or βIVb-tubulin on PC growth and chemosensitivity. PC cells (MiaPaCa-2, HPAF-II, AsPC1) were treated with siRNA (control, βIVa-tubulin or βIVb-tubulin). The ability of PC cells to form colonies in the presence or absence of chemotherapy was measured by clonogenic assays. Inhibition of βIVa-tubulin in PC cells had no effect chemosensitivity. In contrast, inhibition of βIVb-tubulin in PC cells sensitized to vinca alkaloids (Vincristine, Vinorelbine and Vinblastine), which was accompanied by increased apoptosis and enhanced cell cycle arrest. We show for the first time that βIVb-tubulin, but not βIVa-tubulin, plays a role in regulating vinca alkaloid chemosensitivity in PC cells. The results from this study suggest βIVb-tubulin may be a novel therapeutic target and predictor of vinca alkaloid sensitivity for PC and warrants further investigation.

3 Article VEGF Promotes Glycolysis in Pancreatic Cancer via HIF1α Up-Regulation. 2016

Shi, S / Xu, J / Zhang, B / Ji, S / Xu, W / Liu, J / Jin, K / Liang, D / Liang, C / Liu, L / Liu, C / Qin, Y / Yu, X. ·Department of Oncology, Shanghai Medical College, Fudan University; Pancreatic Cancer Institute, Fudan University, 270 DongAn Road, Shanghai 200032, China. qinyi@fudanpci.org. · Department of Pancreatic and Hepatobiliary Surgery, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University; Pancreatic Cancer Institute, Fudan University, 270 DongAn Road, Shanghai 200032, China. yuxianjun88@hotmail.com. ·Curr Mol Med · Pubmed #26980697.

ABSTRACT: BACKGROUND: Vascular endothelial growth factor (VEGF) is highly expressed in many types of tumors, including pancreatic cancer. Tumor cellderived VEGF promotes angiogenesis and tumor progression. However, the role of VEGF in glucose metabolism remains unclear. OBJECTIVE: We investigated the role and the underlying mechanism of VEGF in the glucose metabolism of pancreatic cancer cells. METHOD: Pancreatic cancer cells were stimulated with VEGF165 for 1 or 2 h. The oxygen consumption rates (OCR) and extracellular acidification rates (ECAR) were measured using the Seahorse XF96 Extracellular Flux Analyzer. Glycolytic enzymes were detected by quantitative real-time PCR. Neuropilin 1 (NRP1) was silenced by shRNA in order to investigate its role in VEGF-induced glycolysis. Immunohistochemistry (IHC) was performed to identify the correlation among VEGF, NRP1 and hypoxia inducible factor 1α (HIF1α) in pancreatic cancer tissues. RESULTS: VEGF stimulation led to a metabolic transition from mitochondrial oxidative phosphorylation to glycolysis in pancreatic cancer. HIF1α and NRP1 protein levels were both increased after VEGF stimulation. The down-regulation of NRP1 reduced glycolysis in pancreatic cancer cells. NRP1 and VEGF levels both correlated with HIF1α expression in pancreatic tumor tissues. CONCLUSION: VEGF enhances glycolysis in pancreatic cancer via HIF1α up-regulation. NRP1 plays a key role in VEGF-induced glycolysis.

4 Article MBD1 is an Epigenetic Regulator of KEAP1 in Pancreatic Cancer. 2016

Zhang, B / Xu, J / Li, C / Shi, S / Ji, S / Xu, W / Liu, J / Jin, K / Liang, D / Liang, C / Liu, L / Liu, C / Qin, Y / Yu, X. ·Department of Oncology, Shanghai Medical College, Fudan University; Pancreatic Cancer Institute, Fudan University, 270 DongAn Road, Shanghai 200032, China. qinyi@fudanpci.org. · Department of Pancreatic and Hepatobiliary Surgery, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University; Pancreatic Cancer Institute, Fudan University, 270 DongAn Road, Shanghai 200032, China. yuxianjun88@hotmail.com. ·Curr Mol Med · Pubmed #26980696.

ABSTRACT: BACKGROUND: MBD1 (Methyl-CpG Binding Domain Protein 1) is highly expressed in pancreatic cancer. Nrf2 (NF-E2 p45-related factor 2) and the 'antioxidant response element' (ARE)-driven genes that NRF2 controls are frequently upregulated in pancreatic cancer and correlate with poor survival. Keap1 (Kelch-like ECH-associated protein 1) is a dominant negative regulator of NRF2 and is reported to be epigenetically regulated by promoter methylation. However, the role of MBD1 with antioxidant response and its association with KEAP1 has never been reported before and remains unclear. OBJECTIVE: We investigated the role of MBD1 in antioxidant response and its regulatory function in KEAP1 transcription in pancreatic cancer cells. METHOD: MBD1 was silenced to examine its role in antioxidant response. To explore the underlying mechanism, transcriptional and protein levels of KEAP1 was examined. The correlation between MBD1 and KEAP1 was confirmed in pancreatic cancer tissue samples by using immunohistochemistry (IHC). Dualluciferase reporter assay and Chromatin immunoprecipitation (ChIP) were used to elucidate he mechanism of MBD1 in KEAP1 transcriptional control. Moreover, co-immunoprecipitation (CoIP) assay was performed to uncover the regulatory role of MBD1 in KEAP1 transcription through its association with c-myc. RESULTS: MBD1 silencing decreased antioxidant response and the related ARE target genes through epigenetic regulation of KEAP1. MBD1 negatively correlated with KEAP1 in pancreatic cancer tissue samples. Moreover, c-myc was a MBD1 interaction partner in KEAP1 epigenetic regulation. CONCLUSION: MBD1 can induce antioxidant response in pancreatic cancer through down-regulation of KEAP1. c-myc plays a key role in MBD1 mediated epigenetic silencing of KEAP1.

5 Article A case-control study indicates that the TRIB1 gene is associated with pancreatic cancer. 2014

Lu, X X / Hu, J J / Fang, Y / Wang, Z T / Xie, J J / Zhan, Q / Deng, X X / Chen, H / Jin, J B / Peng, C H / Liu, J / Li, H W / Shen, B Y. ·Department of General Surgery, Rui-Jin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China. · Department of Nuclear Medicine, Rui-Jin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China. · Department of Gastroenterology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China. · Shanghai Institute of Orthopaedics and Traumatology, Rui-Jin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China. · Department of General Surgery, Rui-Jin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China byshen_rjh@126.com. ·Genet Mol Res · Pubmed #25117373.

ABSTRACT: Pancreatic cancer is a malignant neoplasm originating from transformed cells arising in tissues that form the pancreas. To investigate whether the tribbles homolog 1 (Drosophila) gene (TRIB1) is associated with pancreatic cancer in the Chinese Han population, we conducted this case-control study and genotyped 3 single nucleotide polymorphisms (rs2980879, rs2980874, and rs2235108) of the TRIB1 gene in 182 patients and 359 normal controls of Chinese Han origin and analyzed their association. The results showed that the rs2980879 polymorphism was associated with pancreatic cancer [allele: P = 0.023434, genotype: P = 0.03005; odds ratio (OR) and 95% confidence interval (CI) = 0.727788 (0.552664-0.958404)], whereas the rs2980874 polymorphism had no association with pancreatic cancer [allele: P = 0.749885, genotype: P = 0.699533; OR and 95%CI = 1.041981 (0.809196-1.341734)], and the rs2235108 polymorphism was not associated with the disease [allele: P = 0.629475, genotype: P = 0.547534, OR and 95%CI = 1.128290 (0.690829-1.842770)]. Haplotype analyses and linkage disequilibrium tests were also conducted, and the results showed that these 3 loci are not in the same block. In conclusion, our study indicated that the TRIB1 gene is associated with pancreatic cancer. More studies with larger samples are needed in order to support this finding.

6 Article β2-AR-HIF-1α: a novel regulatory axis for stress-induced pancreatic tumor growth and angiogenesis. 2013

Shan, T / Ma, J / Ma, Q / Guo, K / Guo, J / Li, X / Li, W / Liu, J / Huang, C / Wang, F / Wu, E. ·Department of Hepatobiliary Surgery, First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, China. ·Curr Mol Med · Pubmed #23745588.

ABSTRACT: The purpose of this study was to test the hypothesis that chronic stress in a negative social and psychological state plays a critical role in pancreatic cancer development and progression. In this study, we created a new stress model system to determine the effects of chronic stress on pancreatic cancer progression. Here, we show that chronic stress not only causes depression in mice, most likely attributed to an elevated level of epinephrine, but also induces pancreatic cancer progression. We provide evidence that the pancreatic cancer progression induced by chronic stress could be blocked to a significant degree by β2-AR inhibitor ICI118 551 or HIF-1α inhibitor 2-methoxyestradiol. Moreover, establishment of pancreatic cancer in mice exposed to chronic stress was accompanied by up-regulation of the expression of MMP-2, MMP-9, and VEGF, mediated by a HIF- 1α-dependent β-AR signaling pathway. Our data suggest that the β2-AR-HIF-1α axis regulates stress-induced pancreatic tumor growth and angiogenesis. This study may have a therapeutic or preventive potential for the patients with pancreatic cancer who are especially prone to psychosocial stress challenges.

7 Article Role of Rac1-dependent NADPH oxidase in the growth of pancreatic cancer. 2011

Du, J / Liu, J / Smith, B J / Tsao, M S / Cullen, J J. ·Department of Radiation Oncology, University of Iowa College of Medicine, Iowa City, IA, USA. ·Cancer Gene Ther · Pubmed #21037555.

ABSTRACT: K-ras mutations occur in as high as 95% of patients with pancreatic cancer. K-ras activates Rac1-dependent NADPH oxidase, a key source of superoxide. Superoxide has an important function in pancreatic cancer cell proliferation, and scavenging or decreasing the levels of superoxide inhibits pancreatic cancer cell growth both in vitro and in vivo. DNA microarray analysis and RT-PCR has demonstrated that Rac1 is also upregulated in pancreatic cancer. The aim of this study was to determine whether inhibiting Rac1 would alter pancreatic tumor cell behavior. Human pancreatic cancer cells with mutant K-ras (MIA PaCa-2), wild-type K-ras (BxPC-3) and the immortal H6c7 cell line (pancreatic ductal epithelium) expressing K-ras oncogene (H6c7eR-KrasT) that is tumorigenic, were infected with a dominant/negative Rac1 construct (AdN17Rac1). In cells with mutant K-ras, AdN17Rac1 decreased rac activity, decreased superoxide levels and inhibited in vitro growth. However, in the BxPC-3 cell line, AdN17Rac1 did not change rac activity, superoxide levels or in vitro cell growth. Additionally, AdN17Rac1 decreased superoxide levels and inhibited in vitro growth in the KrasT tumorigenic cell line, but had no effect in the immortalized H6c7 cell line. In human pancreatic tumor xenografts, intratumoral injections of AdN17Rac1 inhibited tumor growth. These results suggest that activation of Rac1-dependent superoxide generation leads to pancreatic cancer cell proliferation. In pancreatic cancer, inhibition of Rac1 may be a potential therapeutic target.