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Experimental cell research 24건

  1. [해외논문]   Establishment of twist-1 and TGFBR2 as direct targets of microRNA-20a in mesenchymal to epithelial transition of breast cancer cell-line MDA-MB-231   SCI SCIE

    De, Soumasree (Corresponding author.) , Das, Sayantani , Mukherjee, Srimoyee , Das, Sainy , Sengupta (Bandyopadhyay), Sumita
    Experimental cell research v.361 no.1 ,pp. 85 - 92 , 2017 , 0014-4827 ,

    초록

    Abstract Messenchymal to epithelial transition (MET) is a significant physiological phenomenon involved in embryogenesis and cancer. This study aims at investigating the mechanism of microRNA-20a (miR-20a) mediated regulation of mesenchymal to epithelial transition and identification of its direct target genes in breast cancer cell-line, MDA-MB-231. Reduced migratory and invasive property, altered cellular morphology along with reduced capability for attachment to basement membrane was acquired by over-expression of miR-20a in invasive MDA-MB-231 cell-line initially expressing low level of this micro-RNA, indicating direct correlation between abundance of miR-20a and metastatic property. The switch from mesenchymal to epithelial cells mediated by miR-20a involved post-transcriptional down-regulation of twist1 , which in turn controls downstream epithelial markers like E-cadherin, claudin and mesenchymal markers like N-cadherin, fibronectin, the crucial players of mesenchymal to epithelial transition (MET). Furthermore, another key component, TGF-β and one of its receptors (TGFBR2) were found to be down-regulated by miR-20a. Additionally, reporter assay established that post-transcriptional down-regulation of TGFBR2 occurred through direct binding of miR-20a to its 3′UTR, thus abrogating the TGF-β signaling pathway resulting in inhibition of MET. Delineating the underlying molecular mechanism of miR-20a-mediated MET and defining the target genes will help us to introduce a miRNA-mediated effective therapeutic strategy against breast cancer. Highlights Metastatic property and miR-20a level is directly correlated in MDA-MB-231 cell-line. Over-expression of miR-20a down-regulates expression of twist1. twist1 upregulates crucial epithelial markers and down-regulates mesenchymal markers. TGF-β and its receptor, TGFBR2 were found to be targets of miR-20a.

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  2. [해외논문]   Biomechanical strain-induced modulation of proliferation coincides with an ERK1/2-independent nuclear YAP localization   SCI SCIE

    Hü (Department of Orthodontics, Medical Center –) , lter-Hassler, Diana (University of Freiburg, Faculty of Medicine, University of Freiburg, Hugstetter Str. 55, 79106 Freiburg, Germany ) , Wein, Martin (Faculty of Biology, University of Freiburg, Schaenzlestr. 1, 79104 Freiburg, Germany ) , Schulz, Simon D. (Department of Oral Biotechnology, Medical Center –) , Proksch, Susanne (University of Freiburg, Faculty of Medicine, University of Freiburg, Hugstetter Str. 55, 79106 Freiburg, Germany ) , Steinberg, Thorsten (Department of Operative Dentistry and Periodontology, Medical Center –) , Jung, Britta A. (University of Freiburg, Faculty of Medicine, University of Freiburg, Hugstetter Str. 55, 79106 Freiburg, Germany ) , Tomakidi, Pascal (Department of Oral Biotechnology, Medical Center –)
    Experimental cell research v.361 no.1 ,pp. 93 - 100 , 2017 , 0014-4827 ,

    초록

    Abstract Biomechanical strain induces activation of the transcriptional co-activator yes-associated protein (YAP) by nuclear re-distribution. Recent findings indicate that the mechanically responsive mitogen-activated protein kinase (MAPK) extracellular signal-regulated kinase (ERK) 1/2 is involved in the amount of nuclear YAP, reflecting its activation. In this context, we conducted experiments to detect how biomechanical strain acts on the subcellular localization of YAP in periodontal cells. To this end, cells were subjected to 2.5% static equiaxial strain for different time periods. Western blot and fluorescence imaging-based analyses revealed a clear modulation of nuclear YAP localization. This modulation fairly coincided with the altered course of the KI-67 protein amount in conjunction with the percentage of KI-67-positive and thus proliferating cells. The inhibition of the ERK1/2 activity via U0126 yielded an unchanged strain-related modulation of nuclear YAP localization, while YAP amount in whole cell extracts of strained cells was decreased. Administration of the YAP-inhibiting drug Verteporfin evoked a clear reduction of KI-67-positive and thus proliferating cells by approximately 65%, irrespective of strain. Our data reveal YAP as a regulator of strain-modulated proliferation which occurs in a MAPK-independent fashion. Highlights Strain-induced modulation of nuclear YAP amount coincides with proliferation. YAP-inhibiting drug Verteporfin yields distinct reduction of KI-67-positive cells. This demonstrates regulatory involvement of nuclear YAP in proliferation. Strain-induced YAP modulation is mechanistically independent from ERK1/2 activity. ERK1/2 activity influences total YAP amount, exclusively in strained cells. Graphical abstract [DISPLAY OMISSION]

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  3. [해외논문]   Effects of retinoic acid signaling on extraocular muscle myogenic precursor cells in vitro   SCI SCIE

    Hebert, Sadie L. (Department of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, MN, United States ) , Fitzpatrick, Krysta R. (Department of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, MN, United States ) , McConnell, Samantha A. (Department of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, MN, United States ) , Cucak, Anja (Department of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, MN, United States ) , Yuan, Ching (Department of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, MN, United States ) , McLoon, Linda K. (Department of Ophthalmology and Visual Neurosciences, University of Minnesota, Minneapolis, MN, United States)
    Experimental cell research v.361 no.1 ,pp. 101 - 111 , 2017 , 0014-4827 ,

    초록

    Abstract One major difference between limb and extraocular muscles (EOM) is the presence of an enriched population of Pitx2-positive myogenic precursor cells in EOM compared to limb muscle. We hypothesize that retinoic acid regulates Pitx2 expression in EOM myogenic precursor cells and that its effects would differ in leg muscle. The two muscle groups expressed differential retinoic acid receptor (RAR) and retinoid X receptor (RXR) levels. RXR co-localized with the Pitx2-positive cells but not with those expressing Pax7. EOM-derived and LEG-derived EECD34 cells were treated with vehicle, retinoic acid, the RXR agonist bexarotene, the RAR inverse agonist BMS493, or the RXR antagonist UVI 3003. In vitro , fewer EOM-derived EECD34 cells expressed desmin and fused, while more LEG-derived cells expressed desmin and fused when treated with retinoic acid compared to vehicle. Both EOM and LEG-derived EECD34 cells exposed to retinoic acid showed a higher percentage of cells expressing Pitx2 compared to vehicle, supporting the hypothesis that retinoic acid plays a role in maintaining Pitx2 expression. We hypothesize that retinoic acid signaling aids in the maintenance of large numbers of undifferentiated myogenic precursor cells in the EOM, which would be required to maintain EOM normalcy throughout a lifetime of myonuclear turnover. Highlights Eye and leg muscle express different RAR and RXR levels. Pitx2+ myogenic precursor cells in extraocular muscles express the RXR receptor. RA alters rates of Pitx2+ cell proliferation and differentiation. Increased RA signaling increased numbers of Pitx2+ cells in vitro . Pitx2+ cells from extraocular and limb muscles respond differently to RA treatment. Graphical abstract [DISPLAY OMISSION]

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  4. [해외논문]   Regulation of HC11 mouse breast epithelial cell differentiation by the E-cadherin/Rac axis   SCI SCIE

    Niit, Maximilian (Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada K7L 3N6 ) , Arulanandam, Rozanne (Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada K7L 3N6 ) , Cass, Jamaica (Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada K7L 3N6 ) , Geletu, Mulu (Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada K7L 3N6 ) , Hoskin, Victoria (Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada K7L3N6 ) , Cô (Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada K7L 3N6 ) , té (Department of Chemical and Physical Sciences, University of Toronto, Mississauga, Ontario, Canada L5L 1C6 ) , , Graham (Department of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada K7L3N6 ) , Gunning, Patrick (Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada K7L 3N6) , Elliott, Bruce , Raptis, Leda
    Experimental cell research v.361 no.1 ,pp. 112 - 125 , 2017 , 0014-4827 ,

    초록

    Abstract It was previously demonstrated that differentiation of some established breast epithelial cell lines requires confluence and stimulation with hydrocortisone, insulin and prolactin inducers. We and others previously demonstrated that E-cadherin engagement, which is favored under conditions of confluence, increases the levels and activity of the Rac small GTPase. To investigate the functional relationship between the transforming ability of Rac and its role as an integral component of the differentiative E-cadherin signaling pathway, we introduced a mutationally activated form of Rac, Rac V12 , into the mouse breast epithelium-derived cell line, HC11. Our results demonstrate that the strength of the Rac signal is key for the outcome of the differentiation process; cRac1 is critically required for differentiation, and at low levels, mutationally activated Rac V12 is able to in crease differentiation, presumably reinforcing the E-cadherin/Rac differentiative signal. However, high Rac V12 expression blocked differentiation concomitant with E-cadherin downregulation, while inducing neoplastic transformation. Therefore, the intensity of the Rac signal is a central determinant in the balance between cell proliferation vs differentiation, two fundamentally opposed processes, a finding which could also have important therapeutic implications.

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  5. [해외논문]   High YBX1 expression indicates poor prognosis and promotes cell migration and invasion in nasopharyngeal carcinoma   SCI SCIE

    Zhou, Lei-lei (Department of Oncology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu, China ) , Ni, Jie (Nanjing Medical University Affliated Cancer Hospital, Department of Clinical Cancer Research Center, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing, Jiangsu, China ) , Feng, Wan-ting (Department of Oncology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu, China ) , Yao, Rong (Department of Oncology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu, China ) , Yue, Shun (Department of Oncology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu, China ) , Zhu, Ya-ning (Department of Pathology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu, China ) , Tang, Hai-yan (Department of Pathology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu, China ) , Lv, Ling-yun (Department of Otolaryngology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, Jiangsu, China ) , Feng, Ji-feng (Nanjing Medical Universit) , Zhu, Wei-guo
    Experimental cell research v.361 no.1 ,pp. 126 - 134 , 2017 , 0014-4827 ,

    초록

    Abstract Y-box binding protein-1 (YBX1) is a multifunctional protein and often acts as an indicator of poor prognosis in cancers. Increasing evidence has shown that the levels of YBX1 protein were closely associated with multidrug resistance, relapse, metastasis and poor prognosis in cancers. However, its role in nasopharyngeal carcinoma (NPC) metastasis remains unknown. In our study, we discovered that the expression of YBX1 was increased in nasopharyngeal carcinoma tissues. YBX1 protein levels positively correlated with T stage and metastasis of NPC patients. Moreover, expression of YBX1 was negatively correlated with membrane E-cadherin levels and positively correlated with Vimentin expression. In vitro, the expression of YBX1 was closely related to the invasive and migratory ability of nasopharyngeal carcinoma cells. Knockdown of YBX1 inhibited migration and invasion in 5–8F cells, and over-expression of YBX1 promoted CNE1 cells migration and invasion. Transforming growth factor-β1 (TGF-β1) treatment led to epithelial-to-mesenchymal transition (EMT) in CNE1 cells accompanied by elevated YBX1 expression. On the contrary, knockdown of YBX1 partially inhibited the TGF-β1-induced CNE1 cell migration, together with changes of EMT-associated markers. Our study revealed that TGF-β1/YBX1 signaling might be one of novel mechanisms mediating EMT in NPC, providing a new target for the treatment of nasopharyngeal carcinoma. Highlights YBX1 overexpressed in cytoplasmic of nasopharyngeal carcinoma cells. YBX1 expression associated with the EMT process in nasopharyngeal carcinoma. TGF-β1 induced YBX1 expression in NPC cell lines. TGF-β1/YBX1 signaling mediated the EMT process in NPC cell lines.

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  6. [해외논문]   Fecal bacteria from treatment-naive Crohn's disease patients can skew helper T cell responses   SCI SCIE

    Ma, Fei (Department of Oncology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China ) , Zhang, Yi (Department of Digestive Endoscopic Diagnosis and Treatment, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China ) , Xing, Junjie (Department of Colorectal Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China ) , Song, Xiaoling (Department of Colorectal Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China ) , Huang, Ling (Department of Colorectal Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China ) , Weng, Hao (Department of Colorectal Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China ) , Wu, Xiangsong (Department of Colorectal Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China ) , Walker, Emma (DICAT Biomedical Computation Centre, Vancouver, Canada ) , Wang, Zhongchuan (Department of Colorectal Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, Ch)
    Experimental cell research v.361 no.1 ,pp. 135 - 140 , 2017 , 0014-4827 ,

    초록

    Abstract Many studies have demonstrated that the inflamed mucosa of Crohn's disease (CD) patients presented a disturbed gut commensal community, and the shift in microbial composition and species variety is associated with disease severity. To establish a link between changes in the intestinal bacterial composition and the alteration of inflammation, we obtained fecal bacteria from CD patients and non-CD controls. The bacteria were then used to stimulate the peripheral blood mononuclear cells (PBMCs) from one non-CD individual. We found that the frequency of IFN-γ- and IL-17-expressing CD4 T cells was significantly higher after stimulation with CD bacteria than with non-CD bacteria, while the frequency of IL-4- and IL-10-expressing CD4 T cells was significantly decreased after stimulation with CD bacteria. A similar trend was observed in the level of cytokine expression and transcription expression. However, this difference was not clear-cut, as overlapping regions were observed between the two groups. With longer stimulation using CD bacteria, the skewing toward Th1/Th17 responses were further increased. This increase depended on the presence of monocytes/macrophages. Interestingly, we also found that B cells presented an inhibitory effect in CD bacteria-mediated skewing toward Th1/Th17 cells and promoted IL-10 secretion in CD bacteria-stimulated PBMCs. Together, our results demonstrated that CD bacteria could promote Th1/Th17 inflammation in a host factor-independent fashion.

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  7. [해외논문]   Chondrocytes damage induced by T-2 toxin via Wnt/β-catenin signaling pathway is involved in the pathogenesis of an endemic osteochondropathy, Kashin-Beck disease   SCI SCIE

    Wang, Xi (School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, Shaanxi 710061, PR China ) , Ning, Yujie (School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, Shaanxi 710061, PR China ) , Zhang, Pan (School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, Shaanxi 710061, PR China ) , Yang, Lei (School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, Shaanxi 710061, PR China ) , Wang, Yingting (School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and) , Guo, Xiong
    Experimental cell research v.361 no.1 ,pp. 141 - 148 , 2017 , 0014-4827 ,

    초록

    Abstract Kashin-Beck disease (KBD), an endemic osteochondropathy, is characterized by cartilage degeneration which is caused by abnormal catabolism in the extracellular matrix (ECM). In this study, we investigated the expression of the Wnt/β-catenin signaling pathway in KBD pathogenesis. Among the proteins involved in the Wnt/β-catenin signaling pathway, WNT-3A, FZD1, SOX9, and β-catenin were up-regulated, while FRZB was down-regulated in KBD cartilage. C28/I2 cells were evaluated for cell viability using the MTT assay after exposure to T-2 toxin, a suspicious environmental pathogenic factors of KBD. C28/I2 cells were treated with different intervening concentrations (0.001μg/mL,0.005μg/mL and 0.01μg/mL) of T-2 toxin for 24h. The expression of FZD1 and CTNNB1 (i.e.,β-catenin) was significantly reduced and SOX9 expression was significantly increased in chondrocytes after treatment with different intervening concentrations of T-2 toxin. Our results indicate that alterations in the Wnt/β-catenin signaling pathway in articular cartilage play an important role in the onset and pathogenesis of KBD. Highlights Wnt/β-catenin signaling pathway involve in the pathogenesis of KBD. T-2 toxin lead to cartilage injury through alterations in the Wnt/β-catenin signaling pathway. Wnt/β-catenin signaling pathway was abnormally activated in juvenile KBD patients and degraded in adult KBD patients.

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  8. [해외논문]   CD21lo/medCD27+ proinflammatory B cells are enriched in breast cancer patients and promote antitumor T cell responses   SCI SCIE

    Zhu, Shiguang (Corresponding author.) , Wang, Xingmiao , Wang, Ji , Lin, Jun , Cong, Yizi , Qiao, Guangdong
    Experimental cell research v.361 no.1 ,pp. 149 - 154 , 2017 , 0014-4827 ,

    초록

    Abstract Breast cancer is a common malignancy and a major cause of death in women worldwide. The immunomodulatory role of B cells is being increasingly recognized in autoimmune diseases and cancers. In recent years, immunotherapeutic strategies that upregulate the patient's own antitumor T cell responses have shown promise in treating solid tumors and are being developed for breast cancer. In this study, we discovered that the B cells in breast cancer patients were enriched with interferon (IFN)-γ-expressing cells and presented high potency for IFN-γ production. These IFN-γ-expressing B cells were enriched in, but did not completely overlap with, the CD21 lo/med CD27 + IgM - IgD - IgG + IgA - B cell subset, which was consistent with IgG-expressing memory B cells. Compared to CD27 + IgG - B cells, the CD27 + IgG + B cells expressed significantly higher IFN-γ expression. Given that B cells demonstrate important antigen-presenting function to T cells, we incubated CD27 + IgG - B cells and CD27 + IgG + B cells with autologous CD4 + T cells. Compared to the CD4 + T cells that were incubated with CD27 + IgG - B cells, the CD4 + T cells that were incubated with CD27 + IgG + B cells presented significantly higher TBX21 and lower FOXP3 expression, suggesting that the CD27 + IgG + B cells, but not the CD27 + IgG - B cells, promoted Th1 and suppressed regulatory T cell responses. IFN-γ-expressing B cells were further enriched in the intratumoral environment of breast cancer patients. Together, we discovered that breast cancer patients presented an upregulation of IFN-γ-expressing proinflammatory B cells with the potency to promote Th1 responses.

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  9. [해외논문]   The histone demethylase JMJD2A regulates the expression of BDNF and mediates neuropathic pain in mice   SCI SCIE

    Zhou, Junfei (Department of Anesthesiology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China ) , Wang, Fang (Department of Pain Management, Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China ) , Xu, Chang (Department of Anesthesiology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China ) , Zhou, Zipeng (Department of Rheumatology, Henan Province Hospital of TCM, Zhengzhou, China ) , Zhang, Wei (Department of Anesthesiology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China)
    Experimental cell research v.361 no.1 ,pp. 155 - 162 , 2017 , 0014-4827 ,

    초록

    Abstract JMJD2A is a JmjC histone demethylase that catalyzes the demethylation of di- and trimethylated Lys9 and Lys36 in histone H3 (H3K9me2/3 and H3K36me2/3). The role of spinal JMJD2A-dependent histone demethylation in nociception hypersensitivity development remains elusive. Here we reported that the JMJD2A responded to neuropathic pain and participated in the maintenance of neuropathic pain. The mRNA and protein levels of Jmjd2a were significantly increased in the neurons of mouse undergoing neuropathic pain induced by sciatic nerve chronic constrictive injury (CCI) or unilateral spared nerve injury (SNI). Jmjd2a responded to 5-hydroxytryptamine (5-HT) and promoted the expression of the brain-derived neurotrophic factor ( Bdnf ), which is a protein critically involved in neuropathic pain. JMJD2A bound to the promoter of Bdnf and demethylated H3K9me3 and H3K36me3 at Bdnf promoter to promote the expression of Bdnf. Finally, we showed that JMJD2A promoted the expression of Bdnf during neuropathic pain and neuron-specific knockout of Jmjd2a blocked the hypersensitivity of mice undergoing chronic neuropathic pain induced by CCI and SNI. Taken together, our findings demonstrate that up-regulation of JMJD2A promotes neuropathic pain and it may serve as a promising target for treatment of chronic neuropathic pain. Highlights JMJD2A is upregulated during chronic neuropathic pain. JMJD2A is regulated by 5-hydroxytryptamine (5-HT). JMJD2A promotes the expression of brain-derived neurotrophic factor (Bdnf) . JMJD2A regulates the levels of H3K9me3 and H3K36me3 at the promoter of Bdnf . JMJD2A regulates Bdnf to participate in chronic neuropathic pain.

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  10. [해외논문]   CCN1 sensitizes esophageal cancer cells to TRAIL-mediated apoptosis   SCI SCIE

    Dang, Tong (The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, 30 Hudemulin Rd, Baotou 014030, China ) , Modak, Cristina (Laboratory of Gastrointestinal Injury and Cancer, VA Long Beach Healthcare System, Long Beach, CA 90822, USA ) , Meng, Xiemei (The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, 30 Hudemulin Rd, Baotou 014030, China ) , Wu, Jinbao (The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, 30 Hudemulin Rd, Baotou 014030, China ) , Narvaez, Reinier (Laboratory of Gastrointestinal Injury and Cancer, VA Long Beach Healthcare System, Long Beach, CA 90822, USA ) , Chai, Jianyuan (The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science and Technology, 30 Hudemulin Rd, Baotou 014030, China)
    Experimental cell research v.361 no.1 ,pp. 163 - 169 , 2017 , 0014-4827 ,

    초록

    Abstract TRAIL is one of the best anti-cancer molecules in our body. It kills a variety of cancer cells that are resistant to conventional chemotherapy, without causing much negative impact on normal cells, because its death receptors are almost exclusively found on cancer cells. However, some cancer cells are not sensitive to TRAIL treatment, even though they express its death receptors. A second molecule is needed to help TRAIL to complete its mission. Finding such molecules now becomes a top priority in cancer research. Our study shows that CCN1 is such a molecule. CCN1 was highly expressed in the esophageal epithelium of the patients suffering from gastroesophageal reflux disease, but faded away as the situation worsened towards adenocarcinoma. Treating the tumor cells with CCN1 resulted in apoptosis, while the same treatment to the normal cells only nourished cell growth. It was TRAIL that mediated this process. Apparently, CCN1 altered the expression profile of TRAIL and its receptors in tumor cells, namely, activating TRAIL and its death receptors and shutting down its decoy receptors. CCN1 and TRAIL worked as a team to put the cancer cells to death, as elimination of either one failed apoptosis. Highlights EAC cells express all three decoy receptors of TRAIL. CCN1 is barely detectable in EAC cells. CCN1 inhibits expression of TRAIL decoy receptors in EAC cells. CCN1 induces apoptosis in EAC cells. TRAIL mediates CCN1-induced EAC cell apoptosis. Graphical abstract [DISPLAY OMISSION]

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