Dalian Medical University

About: Dalian Medical University is a education organization based out in Dalian, China. It is known for research contribution in the topics: Cancer & Apoptosis. The organization has 15623 authors who have published 9993 publications receiving 164145 citations.

Cancer-associated fibroblasts promote non-small cell lung cancer cell invasion by upregulation of glucose-regulated protein 78 (GRP78) expression in an integrated bionic microfluidic device

Abstract: // Ting Yu 1, * , Zhe Guo 1, * , Hui Fan 2, * , Jing Song 1 , Yuanbin Liu 1, 3 , Zhancheng Gao 4 , Qi Wang 1 1 Department of Respiratory Medicine, The Second Hospital, Dalian Medical University, Dalian, China 2 Department of Oncology, The Second Hospital, Dalian Medical University, Dalian, China 3 Key Laboratory of Laboratory Medicine, Ministry of Education, Zhejiang Provincial Key Laboratory of Medical Genetics, Wenzhou Medical University, Wenzhou, China 4 Department of Respiratory & Critical Care Medicine, the People’s Hospital of Peking University, Beijing, China * These authors have contributed equally to this work Correspondence to: Qi Wang, e-mail: wqdlmu@163.com Zhancheng Gao, e-mail: gaozhancheng5446@163.com Keywords: cancer-associated fibroblasts, lung cancer, invasion, GRP78, microfluidic chip Received: January 09, 2016 Accepted: March 04, 2016 Published: March 21, 2016 ABSTRACT The tumor microenvironment is comprised of cancer cells and various stromal cells and their respective cellular components. Cancer-associated fibroblasts (CAFs), a major part of the stromal cells, are a key determinant in tumor progression, while glucose-regulated protein (GRP)78 is overexpressed in many human cancers and is involved in tumor invasion and metastasis. This study developed a microfluidic-based three dimension (3D) co-culture device to mimic an in vitro tumor microenvironment in order to investigate tumor cell invasion in real-time. This bionic chip provided significant information regarding the role of GRP78, which may be stimulated by CAFs, to promote non-small cell lung cancer cell invasion in vitro. The data showed that CAF induced migration of NSCLC A549 and SPCA-1 cells in this three-dimensional invasion microdevice, which is confirmed by using the traditional Transwell system. Furthermore, CAF induced GRP78 expression in A549 and SPCA-1 cells to facilitate NSCLC cell migration and invasion, whereas knockdown of GRP78 expression blocked A549 and SPCA-1 cell migration and invasion capacity. In conclusion, these data indicated that CAFs might promote NSCLC cell invasion by up-regulation of GRP78 expression and this bionic chip microdevice is a robust platform to assess the interaction of cancer and stromal cells in tumor environment study.

c-Myc downregulation: a critical molecular event in resveratrol-induced cell cycle arrest and apoptosis of human medulloblastoma cells.

Abstract: The correlation of c-Myc expression with resveratrol-induced turnover of medulloblastoma cells was investigated in this study by checking (1) c-Myc expression in medulloblastoma tissues and cell lines (UW228-2 and UW228-3), (2) the in vitro effect of resveratrol on c-Myc expression and (3) the influences of c-Myc inhibition in cell growth and survival Immunohistochemical staining of human medulloblastomas and noncancerous cerebellar tissues revealed that 8 out of 11 tumor tissues (727%) expressed c-Myc, in which 4 cases (50%) showed intensified nuclear labeling RT-PCR, Western blotting, immunocytochemical and immunofluorescence stainings revealed c-Myc downregulation accompanied with growth suppression and apoptosis Flow cytometry analysis showed S phase arrest in resveratrol-treated cell populations Transfection of c-Myc directed antisense oligonucleotides to the cultured medulloblastoma cells could reduce c-Myc expression, inhibit cell growth and arrest the cell cycle at S phase Our results thus for the first time demonstrate that c-Myc downregulation is a critical molecular event of resveratrol-mediated anti-medulloblastoma activity, which is closely associated with growth suppression, cell cycle arrest and apoptosis of medulloblastoma cells

Dynamic signaling for neural stem cell fate determination.

Abstract: Central nervous system (CNS) development starts from neural stem cells (NSCs) which ultimately give rise to the three major cell types (neurons, oligodendrocytes and astrocytes) of the CNS. NSCs are specified in space- and time-related fashions, becoming spatially heterogeneous and generating a progressively restricted repertoire of cell types. Mammalian NSCs produce different cell types at different time points during development under the influence of multiple signaling pathways. These pathways act in a dynamic web mode to determine the fate of NSCs via modulating the expression and activity of distinct set of transcription factors which in turn trigger the transcription of neural fate-associated genes. This review thus introduces the major signal pathways, transcription factors and their cross-talks and coordinative interactions in NSC fate determination.