کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10156732 | 1666423 | 2018 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Neuroendocrine differentiation contributes to radioresistance development and metastatic potential increase in non-small cell lung cancer
ترجمه فارسی عنوان
تمایز نوروندوکرین موجب افزایش راندگی ریزش و افزایش پتانسیل متاستاز در سرطان ریه های غیر سلولی می شود
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
CGALCNECNEDCREBERKNSEqPCRCREIBMXIL-6cAMP - cAMPCRE binding protein - CRE پروتئین اتصالneuron specific enolase - enolase خاص نورونMTT - MTTPCA - PCACyclic adenosine monophosphate - آدنوزین مونوفسفات CyclicSCLC - بگذارندEnzyme-linked immunosorbent assay - تست الیزاELISA - تست الیزاNeuroendocrine differentiation - تمایز نوروندوکرینEMT - تکنسین فوریتهای پزشکیRadioresistance - رادیاتور مقاومتMEK/ERK - سازمان مجاهدین خلق / ERKNSCLC - سرطان ریوی غیر سلول کوچکSmall cell lung cancer - سرطان سلول کوچک ریهNon-small cell lung cancer - سرطان غیر سلول کوچک ریهProstate cancer - سرطان پروستاتSynaptophysin - سیناپتوفیزینSyn - سینتneuroendocrine - عصبی عضلانیcAMP response element - عنصر پاسخ cAMPquantitative polymerase chain reaction - واکنش زنجیره ای پلیمراز کمیLarge-cell neuroendocrine carcinoma - کارسینوم عصبی عضلانی بزرگ سلولیEpithelial-mesenchymal transition - گذار اپیتلیال-مزانشیمی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
چکیده انگلیسی
Radiation treatment induces neuroendocrine differentiation (NED) in non-small cell lung cancer (NSCLC) A549 and H157 cells, so higher NE-like features in radioresistant A549 (A549R26-1) and H157 (H157R24-1) cells are observed than in parental cells. We detected higher NED marker expressions in A549R26-1 cell-derived tumors than in A549 cell-derived tumors. In mechanism studies, we found that NED induction in A549R26-1 and H157R24-1 cells was accompanied by increased intracellular cAMP and IL-6 levels. Treatment of radioresistant lung cancer cells with the inhibitor (SQ22536) of adenylate cyclase (AC) which is the enzyme responsible for the cAMP production, or the neutralizing antibody (Ab) of IL-6, resulted in decreased NE-like features in radioresistant lung cancer cells. In addition, we found MEK/Erk is the signaling pathway that triggers the cAMP- and IL-6-mediated NED induction in radioresistant lung cancer cells. Also, we found that MEK/Erk signaling pathway inhibition decreased NED in radioresistant cells. Radioresistant lung cancer cells exhibiting high NE-like features also showed higher radioresistance and higher metastatic potential than parental cells. When we inhibited cAMP-, or IL-6-mediated pathways, or the downstream MEK/Erk signaling pathway, radiosensitivity of radioresistant lung cancer cells was significantly increased and their metastatic potential was significantly reduced. In in vivo mouse studies, reducing NED by treating mice with the MEK/Erk inhibitor increased radiosensitivity. Immunohistochemical staining of tumor tissues lowered expressions of the NED/epithelial-mesenchymal transition (EMT)/metastatic markers when mice were treated with the MEK/Erk inhibitor.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1865, Issue 12, December 2018, Pages 1878-1890
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1865, Issue 12, December 2018, Pages 1878-1890
نویسندگان
Rongying Zhu, Xiaodong Yang, Xiang Xue, Mingjing Shen, Feng Chen, Xiaodong Chen, Ying Tsai, Peter C. Keng, Yongbing Chen, Soo Ok Lee, Yuhchyau Chen,