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Sökning: WFRF:(Liu Xisheng)

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1.
  • Cheng, Dantong, et al. (författare)
  • MicroRNA-20a-5p promotes colorectal cancer invasion and metastasis by downregulating Smad4
  • 2016
  • Ingår i: Oncotarget. - : IMPACT JOURNALS LLC. - 1949-2553. ; 7:29, s. 45199-45213
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Tumor metastasis is one of the leading causes of poor prognosis for colorectal cancer (CRC) patients. Loss of Smad4 contributes to aggression process in many human cancers. However, the underlying precise mechanism of aberrant Smad4 expression in CRC development is still little known. Results: miR-20a-5p negatively regulated Smad4 by directly targeting its 3UTR in human colorectal cancer cells. miR-20a-5p not only promoted CRC cells aggression capacity in vitro and liver metastasis in vivo, but also promoted the epithelial-to-mesenchymal transition process by downregulating Smad4 expression. In addition, tissue microarray analysis obtained from 544 CRC patients clinical characters showed that miR-20a-5p was upregulated in human CRC tissues, especially in the tissues with metastasis. High level of miR-20a-5p predicted poor prognosis in CRC patients. Methods: Five miRNA target prediction programs were applied to identify potential miRNA(s) that target(s) Smad4 in CRC. Luciferase reporter assay and transfection technique were used to validate the correlation between miR-20a-5p and Smad4 in CRC. Wound healing, transwell and tumorigenesis assays were used to explore the function of miR-20a-5p and Smad4 in CRC progression in vitro and in vivo. The association between miR-20a-5p expression and the prognosis of CRC patients was evaluated by Kaplan-Meier analysis and multivariate cox proportional hazard analyses based on tissue microarray data. Conclusions: miR-20a-5p, as an onco-miRNA, promoted the invasion and metastasis ability by suppressing Smad4 expression in CRC cells, and high miR-20a-5p predicted poor prognosis for CRC patients, providing a novel and promising therapeutic target in human colorectal cancer.
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2.
  • Cheng, Kaiyuan, et al. (författare)
  • Injectable tricalcium phosphate/calcium sulfate granule enhances bone repair by reversible setting reaction
  • 2021
  • Ingår i: Biochemical and Biophysical Research Communications - BBRC. - : Elsevier. - 0006-291X .- 1090-2104. ; 557, s. 151-158
  • Tidskriftsartikel (refereegranskat)abstract
    • Towards repairing bone defects, calcium sulfate and calcium phosphate cement have been recognized as promising bone grafts. However, the current bone cements are generally lack of proper porosity for cell migration and new tissue formation. On the other hand, porous scaffold cannot be delivered by injection, which limits its use its clinical use. Herein, we develop a novel tricalcium phosphate/calcium sulfate granule to overcome the limitations of injectable cements and traditional scaffolds. The biocompatible granule underwent in situ self-setting to form scaffold with porous structure after injection. It con-tributes to calcium deposition and upregulation of osteogenic genes of mesenchymal stem cells in a time-dependent manner. Within three months, cavitary bone defects of distal rabbit femurs implanted the granules exhibited better bone formation than those with those implanted with autologous bone.
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3.
  • Mi, Yushuai, et al. (författare)
  • miR-181a-5p promotes the progression of gastric cancer via RASSF6-mediated MAPK signalling activation
  • 2017
  • Ingår i: Cancer Letters. - : ELSEVIER IRELAND LTD. - 0304-3835 .- 1872-7980. ; 389, s. 11-22
  • Tidskriftsartikel (refereegranskat)abstract
    • We previously discovered that Ras association domain family member 6 (RASSF6) was downregulated and predicted poor prognosis in GC patients. However, the mechanisms of the down regulation of RASSF6 in GC remained unclear. Increasing evidence indicates that dysregulation of microRNAs promotes the progression of cancer through the repression of tumour suppressors. Here, we identified miR-181a-5p as a novel regulator of RASSF6 in GC. Functionally, ectopic expression or silencing of miR-181a-5p, respectively, promoted or inhibited GC cell proliferation, colony formation and cell cycle transition, as well as enhanced or prevented the invasion, metastasis of GC cells and epithelial to mesenchymal transition of GC cells in vitro and in vivo. Molecularly, miR-181a-5p functioned as an onco-miRNA by activating the RASSF6-regulated MAKP pathway. Overexpression or silencing of RASSF6 could partially reverse the effects of the overexpression or repression of miR-181a-5p on GC progress caused by activation of the MAKP pathway in vitro and in vivo. Clinically, high miR-181a-5p expression predicted poor survival in GC patients, especially combined with low RASSF6 expression. Collectively, we identified miR-181a-5p as an onco-miRNA, which acts by directly repressing RASSF6 in GC. (C) 2017 The Authors. Published by Elsevier Ireland Ltd.
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4.
  • Zhang, Hanzhi, et al. (författare)
  • Quantitative estimation of the contribution of dustsources to Chinese loess using detrital zircon U-Pbage patterns
  • 2016
  • Ingår i: Journal of Geophysical Research - Earth Surface. - 2169-9003 .- 2169-9011. ; 121:11, s. 2085-2099
  • Tidskriftsartikel (refereegranskat)abstract
    • The origin and provenance of the loess deposits of the Chinese Loess Plateau (CLP) are stilldebated. In order to pinpoint the dust sources, surface samples from the piedmont of the NortheasternTibetan Plateau, the Gobi Altai Mountains, and modern eolian dunes from the Tengger desert and Mu Ussand field were analyzed by using the detrital zircon dating technique. In order to quantitatively discriminatethe content of different potential sources, zircon grains of different ages were grouped according to theirtectonic origin. Zircon grains aged from 1300 to 550 Ma were assigned to the Northeastern Tibetan Plateau,and grains aged from 550 to 0 Ma to the Northeastern Tibetan Plateau or the Gobi Altai Mountains, or to acombination of the two. Zircon ages of around 2.8 Ga to 1.3 Ga may be a mixture of sources from theNortheastern Tibetan Plateau, Gobi Altai Mountains, or North China Craton. Sediments from the Tenggerdesert and Mu Us sand field consist of a mixture of the three sources and exhibit a high degree of spatialvariability in terms of their source. In the northern part of the two deserts, 43–83% of the sediments arederived from the Gobi Altai Mountains, while in the south, material from the Northeastern Tibetan Plateaucomprises 51–98% of the sediments. Loess deposits from the CLP also comprise a mixture of the threedifferent sources, with material from the Northeastern Tibetan Plateau making the dominant contribution(65–100%), with material from the North China Craton and the Gobi Altai Mountains comprising 0–35% and0–40% of the loess deposits, respectively. The contributions from the three sources to the loess deposits onCLP vary spatially. Application of the novel statistical method of provenance group analysis demonstratesthat the loess deposits comprise a mixture of material from a broad region of northern China and that theNortheastern Tibetan Plateau material makes the dominant contribution.
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5.
  • Zhao, Senlin, et al. (författare)
  • miR-4775 promotes colorectal cancer invasion and metastasis via the Smad7/TGF beta-mediated epithelial to mesenchymal transition
  • 2017
  • Ingår i: Molecular Cancer. - : BIOMED CENTRAL LTD. - 1476-4598. ; 16
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Despite advancements in the diagnosis and treatment of colorectal cancer (CRC), many patients die because of tumor metastasis or recurrence. Therefore, identifying new prognostic markers and elucidating the mechanisms of CRC metastasis and recurrence will help to improve the prognosis of the disease. As dysregulation of microRNAs is strongly related to cancer progression, the aim of this study was to identify the role of miR-4775 in the prognosis of CRC patients and the underling mechanisms involved in CRC progression. Methods: qPCR and in situ hybridization were used to evaluate the expression of miR-4775 in 544 pairs of paraffin-embedded normal and CRC tissues. Kaplan-Meier analysis with the log-rank test was used for survival analyses. Immunohistochemical staining was applied to investigate the expression of miR-4775-regulated Smad7/TGF beta pathway-associated markers. In vitro and in vivo invasion and metastasis assays were used to explore the function of miR-4775 in the progression of CRC. Results: miR-4775 was identified as a high-risk factor for CRC metastasis and recurrence, with high levels predicting poor survival among the 544 studied CRC patients. Furthermore, high miR-4775 expression promoted the invasion of CRC cells as well as metastasis and the epithelial to mesenchymal transition (EMT) via Smad7-mediated activation of TGF beta signaling both in vitro and in vivo. Downregulating miR-4775 or overexpressing Smad7 reversed the tumor-promoting roles of miR-4775/ Smad7/TGF beta in vitro and in vivo. Conclusion: miR-4775 promotes CRC metastasis and recurrence in a Smad7/TGF beta signaling-dependent manner, providing a new therapeutic target for inhibiting the metastasis or recurrence of the disease.
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