title: Silencing of periostin inhibits nicotine-mediated tumor cell growth             and epithelial-mesenchymal transition in lung cancer cells.
abstract: Nicotine has been found to induce the proliferation of lung cancer cells             through tumor invasion and to confer resistance to apoptosis. Periostin is abnormally             highly expressed in lung cancer and is correlated with angiogenesis, invasion             and metastasis. Here, we investigated the roles of periostin in the lung cancer             cell proliferation, drug resistance, invasion and epithelial-mesenchymal transition             (EMT) induced by nicotine. The periostin gene was silenced using small interfering             RNA (siRNA) in A549 non-small cell lung cancer (NSCLC) cells. The cells were transfected             with control or periostin siRNA plasmids. Periostin mRNA was evaluated by quantitative             reverse transcription-polymerase chain reaction (RT-PCR). Cell proliferation was             detected using the MTT assay and cell apoptosis was detected by Annexin V-FITC             and propidium iodide (PI) double staining. Tumor invasion was detected by the             Boyden chamber invasion assay. Western blotting was performed to detect the expression             of the EMT marker Snail. Our results revealed that stably periostin-silenced cells             were acquired by G418 screening, and the periostin mRNA expression levels of which             were decreased by nearly 80%. Periostin-silenced A549 cells exhibited reduced             cell proliferation, elevated sensitivity to chemotherapy with cisplatin, decreased             cell invasion and Snail expression (P<0.05). Nicotine upregulated the periostin             protein levels in the A549 cells and this upregulation was not blocked by the             generalized nicotinic acetylcholine receptor (nAChR) antagonist, hexamethonium.             In conclusion, periostin is one of the targets regulated by nicotine in lung cancer             cells and is involved in the cancer cell growth, drug resistance, invasion and             EMT induced by nicotine.
authors: Department of Radiation Oncology, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang 310014, PR China. wusqzj@163.com
authors: Shu-Qiang
authors: SQ
authors: Wu
authors: Ya-Er
authors: YE
authors: Lv
authors: Bai-Hua
authors: BH
authors: Lin
authors: Li-Min
authors: LM
authors: Luo
authors: Shi-Liang
authors: SL
authors: Lv
authors: Ai-Hong
authors: AH
authors: Bi
authors: Yong-Shi
authors: YS
authors: Jia
mesh_terms: D000970:Antineoplastic Agents / Q000633:toxicity; D002289:Carcinoma, Non-Small-Cell Lung / Q000378:metabolism / Q000473:pathology; D015815:Cell Adhesion Molecules / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002945:Cisplatin / Q000633:toxicity; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects*; D006801:Humans; D008175:Lung Neoplasms / Q000378:metabolism / Q000473:pathology; D009538:Nicotine / Q000633:toxicity*; D018733:Nicotinic Antagonists / Q000494:pharmacology; D034622:RNA Interference; D012333:RNA, Messenger / Q000378:metabolism; D034741:RNA, Small Interfering / Q000378:metabolism; D011978:Receptors, Nicotinic / Q000737:chemistry / Q000378:metabolism; D000071250:Snail Family Transcription Factors; D014157:Transcription Factors / Q000378:metabolism; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D000970:Antineoplastic Agents; D015815:Cell Adhesion Molecules; D018733:Nicotinic Antagonists; C512835:POSTN protein, human; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D011978:Receptors, Nicotinic; D000071250:Snail Family Transcription Factors; D014157:Transcription Factors; D009538:Nicotine; D002945:Cisplatin