Lentivirus-based RNA Silencing of Nemo-like Kinase (NLK) Inhibits the CAL 27 Human Adenosquamos Carcinoma Cells Proliferation and Blocks G0/G1 Phase to S Phase

The Nemo-like kinase (NLK) is a serine/threonine-protein kinase that involved in a number of signaling pathways regulating cell fate. Variation of NLK has been shown to be associated with the risk of cancer. However, the function of NLK in oral adenosquamous carcinoma cells line CAL-27 is unknown. I...

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Vydané v:	International journal of medical sciences Ročník 10; číslo 10; s. 1301 - 1306
Hlavní autori:	Zhang, Bin, Li, Ke Yi, Chen, Hai Ying, Pan, Shao Dong, Chen, Shuang Feng, Zhang, Wei Feng, Xia, Chun Peng, Jiang, Li Cheng, Liu, Xian Bin, Zhao, Feng Jun, Yuan, Dao Ying, Wang, Le Xin, Wu, Ya Ping, Liu, Shu Wei
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	Australia Ivyspring International Publisher 01.01.2013
Predmet:	Carcinoma, Adenosquamous - enzymology Cell Line, Tumor Cell Proliferation G1 Phase - genetics G1 Phase - physiology Humans Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism Lentivirus - genetics Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism Research Paper Resting Phase, Cell Cycle - genetics Resting Phase, Cell Cycle - physiology RNA Interference - physiology S Phase - genetics S Phase - physiology Oral Squamous Cell Carcinoma RNAi Lentivirus Nemo-like kinase (NLK)
ISSN:	1449-1907, 1449-1907
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Abstract	The Nemo-like kinase (NLK) is a serine/threonine-protein kinase that involved in a number of signaling pathways regulating cell fate. Variation of NLK has been shown to be associated with the risk of cancer. However, the function of NLK in oral adenosquamous carcinoma cells line CAL-27 is unknown. In this study, we evaluated the function of NLK in CAL-27 cells by using lentivirus-mediated RNA silence. The targeted gene expression, cell proliferation and cell cycle are investigated by RT-PCR, western-blot, MTT method, colony forming assay and flow cytometry analysis respectively. After NLK silencing, the number of colonies was significantly reduced (54 ± 5 colonies/well compared with 262 ± 18 colonies/well in non-infected or 226 ± 4 colonies/well in negative control group (sequence not related to NLK sequence with mismatched bases). Using crystal violet staining, we also found that the cell number per colony was dramatically reduced. The RNA silencing of NLK blocks the G0/G1 phase to S phase progression during the cell cycle. These results suggest that NLK silencing by lentivirus-mediated RNA interference would be a potential therapeutic method to control oral squamous carcinoma growth.
AbstractList	The Nemo-like kinase (NLK) is a serine/threonine-protein kinase that involved in a number of signaling pathways regulating cell fate. Variation of NLK has been shown to be associated with the risk of cancer. However, the function of NLK in oral adenosquamous carcinoma cells line CAL-27 is unknown.BACKGROUNDThe Nemo-like kinase (NLK) is a serine/threonine-protein kinase that involved in a number of signaling pathways regulating cell fate. Variation of NLK has been shown to be associated with the risk of cancer. However, the function of NLK in oral adenosquamous carcinoma cells line CAL-27 is unknown.In this study, we evaluated the function of NLK in CAL-27 cells by using lentivirus-mediated RNA silence. The targeted gene expression, cell proliferation and cell cycle are investigated by RT-PCR, western-blot, MTT method, colony forming assay and flow cytometry analysis respectively.METHODSIn this study, we evaluated the function of NLK in CAL-27 cells by using lentivirus-mediated RNA silence. The targeted gene expression, cell proliferation and cell cycle are investigated by RT-PCR, western-blot, MTT method, colony forming assay and flow cytometry analysis respectively.After NLK silencing, the number of colonies was significantly reduced (54 ± 5 colonies/well compared with 262 ± 18 colonies/well in non-infected or 226 ± 4 colonies/well in negative control group (sequence not related to NLK sequence with mismatched bases). Using crystal violet staining, we also found that the cell number per colony was dramatically reduced. The RNA silencing of NLK blocks the G0/G1 phase to S phase progression during the cell cycle.RESULTSAfter NLK silencing, the number of colonies was significantly reduced (54 ± 5 colonies/well compared with 262 ± 18 colonies/well in non-infected or 226 ± 4 colonies/well in negative control group (sequence not related to NLK sequence with mismatched bases). Using crystal violet staining, we also found that the cell number per colony was dramatically reduced. The RNA silencing of NLK blocks the G0/G1 phase to S phase progression during the cell cycle.These results suggest that NLK silencing by lentivirus-mediated RNA interference would be a potential therapeutic method to control oral squamous carcinoma growth.CONCLUSIONSThese results suggest that NLK silencing by lentivirus-mediated RNA interference would be a potential therapeutic method to control oral squamous carcinoma growth. The Nemo-like kinase (NLK) is a serine/threonine-protein kinase that involved in a number of signaling pathways regulating cell fate. Variation of NLK has been shown to be associated with the risk of cancer. However, the function of NLK in oral adenosquamous carcinoma cells line CAL-27 is unknown. In this study, we evaluated the function of NLK in CAL-27 cells by using lentivirus-mediated RNA silence. The targeted gene expression, cell proliferation and cell cycle are investigated by RT-PCR, western-blot, MTT method, colony forming assay and flow cytometry analysis respectively. After NLK silencing, the number of colonies was significantly reduced (54 ± 5 colonies/well compared with 262 ± 18 colonies/well in non-infected or 226 ± 4 colonies/well in negative control group (sequence not related to NLK sequence with mismatched bases). Using crystal violet staining, we also found that the cell number per colony was dramatically reduced. The RNA silencing of NLK blocks the G0/G1 phase to S phase progression during the cell cycle. These results suggest that NLK silencing by lentivirus-mediated RNA interference would be a potential therapeutic method to control oral squamous carcinoma growth. Background: The Nemo-like kinase (NLK) is a serine/threonine-protein kinase that involved in a number of signaling pathways regulating cell fate. Variation of NLK has been shown to be associated with the risk of cancer. However, the function of NLK in oral adenosquamous carcinoma cells line CAL-27 is unknown. Methods: In this study, we evaluated the function of NLK in CAL-27 cells by using lentivirus-mediated RNA silence. The targeted gene expression, cell proliferation and cell cycle are investigated by RT-PCR, western-blot, MTT method, colony forming assay and flow cytometry analysis respectively. Results: After NLK silencing, the number of colonies was significantly reduced (54±5 colonies/well compared with 262±18 colonies/well in non-infected or 226±4 colonies/well in negative control group (sequence not related to NLK sequence with mismatched bases). Using crystal violet staining, we also found that the cell number per colony was dramatically reduced. The RNA silencing of NLK blocks the G0/G1 phase to S phase progression during the cell cycle. Conclusions: These results suggest that NLK silencing by lentivirus-mediated RNA interference would be a potential therapeutic method to control oral squamous carcinoma growth.
Author	Chen, Hai Ying Chen, Shuang Feng Wang, Le Xin Zhang, Wei Feng Pan, Shao Dong Li, Ke Yi Xia, Chun Peng Liu, Shu Wei Wu, Ya Ping Jiang, Li Cheng Yuan, Dao Ying Zhang, Bin Zhao, Feng Jun Liu, Xian Bin
AuthorAffiliation	2. Department of Oral and Maxillofacial Surgery, Liaocheng People's Hospital, Liaocheng Shandong, 252000, P. R. China 1. Department of Anatomy Shandong University, School of Medicine, Jinan Shandong, 250012, P. R. China 4. School of Biomedical Sciences, Charles Sturt University, Wagga Wagga, NSW 2650, Australia 5. Department of Clinical Chemistry and Haematology, University Medical Centre Utrecht, G03.550, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands 3. Key Laboratory of Oral and Maxillofacial-Head and Neck Medicine, Central Laboratory, Liaocheng People's Hospital and Liaocheng Clinical School, Liaocheng Shandong, 252000, P. R. China
AuthorAffiliation_xml	– name: 4. School of Biomedical Sciences, Charles Sturt University, Wagga Wagga, NSW 2650, Australia – name: 5. Department of Clinical Chemistry and Haematology, University Medical Centre Utrecht, G03.550, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands – name: 1. Department of Anatomy Shandong University, School of Medicine, Jinan Shandong, 250012, P. R. China – name: 2. Department of Oral and Maxillofacial Surgery, Liaocheng People's Hospital, Liaocheng Shandong, 252000, P. R. China – name: 3. Key Laboratory of Oral and Maxillofacial-Head and Neck Medicine, Central Laboratory, Liaocheng People's Hospital and Liaocheng Clinical School, Liaocheng Shandong, 252000, P. R. China
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Copyright_xml	– notice: Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited. 2013
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Snippet	The Nemo-like kinase (NLK) is a serine/threonine-protein kinase that involved in a number of signaling pathways regulating cell fate. Variation of NLK has been... Background: The Nemo-like kinase (NLK) is a serine/threonine-protein kinase that involved in a number of signaling pathways regulating cell fate. Variation of...
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SubjectTerms	Carcinoma, Adenosquamous - enzymology Cell Line, Tumor Cell Proliferation G1 Phase - genetics G1 Phase - physiology Humans Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism Lentivirus - genetics Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism Research Paper Resting Phase, Cell Cycle - genetics Resting Phase, Cell Cycle - physiology RNA Interference - physiology S Phase - genetics S Phase - physiology
Title	Lentivirus-based RNA Silencing of Nemo-like Kinase (NLK) Inhibits the CAL 27 Human Adenosquamos Carcinoma Cells Proliferation and Blocks G0/G1 Phase to S Phase
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