Molecular Mechanisms Underlying the Time-dependent Autophagy and Apoptosis Induced by Nutrient Depletion in Multiple Myeloma:a Pilot Study
This study explored the molecular mechanisms underlying the time-dependent autophagy and apoptosis induced by nutrient depletion in human multiple myeloma cell line RPMI8226 cells.RT-PCR and qRT-PCR were used to evaluate the transcriptional levels of Deptor,JNK1,JNK2,JNK3,Raf-1,p53,p21 and NFκB1 at...
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          | Published in | Journal of Huazhong University of Science and Technology. Medical sciences Vol. 32; no. 1; pp. 1 - 8 | 
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| Main Author | |
| Format | Journal Article | 
| Language | English | 
| Published | 
        Heidelberg
          Huazhong University of Science and Technology
    
        01.02.2012
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| Subjects | |
| Online Access | Get full text | 
| ISSN | 1672-0733 1993-1352  | 
| DOI | 10.1007/s11596-012-0001-2 | 
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| Summary: | This study explored the molecular mechanisms underlying the time-dependent autophagy and apoptosis induced by nutrient depletion in human multiple myeloma cell line RPMI8226 cells.RT-PCR and qRT-PCR were used to evaluate the transcriptional levels of Deptor,JNK1,JNK2,JNK3,Raf-1,p53,p21 and NFκB1 at 0,6,12,18,24 and 48 h after nutrient depletion in RPMI8226 cells.We found that transcriptional levels of Deptor were increased time-dependently at 0,6,12 and 18 h,and then decreased.Its alternation was consistent with autophagy.Transcriptional levels of Raf-1,JNK1,JNK2,p53 and p21 were increased time-dependently at 0,6,12,18,24 and 48 h accompanying with the increase of apoptosis.Transcriptional levels of NFκB1 at 6,12,18,24 and 48 h were decreased as com-pared with 0 h.It was suggested that all the studied signaling molecules were involved in cellular re-sponse to nutrient depletion in RPMI8226 cells.Deptor contributed to autophagy in this process.Raf-1/JNK /p53/p21 pathway may be involved in apoptosis,and NFκB1 may play a possible role in in-hibiting apoptosis.It remained to be studied whether Deptor was involved in both autophagy and apoptosis. | 
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| Bibliography: | 42-1679/R ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2  | 
| ISSN: | 1672-0733 1993-1352  | 
| DOI: | 10.1007/s11596-012-0001-2 |