Degradation of p47 by autophagy contributes to CADM1 overexpression in ATLL cells through the activation of NF-κB View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-03-05

AUTHORS

Bidhan Sarkar, Ichiro Nishikata, Shingo Nakahata, Tomonaga Ichikawa, Toshiyuki Shiraga, Hasi Rani Saha, Masahiro Fujii, Yuetsu Tanaka, Kazuya Shimoda, Kazuhiro Morishita

ABSTRACT

Cell adhesion molecule 1 (CADM1), a member of the immunoglobulin superfamily, is identified as a novel cell surface marker for human T-cell leukemia virus (HTLV-1)-infected T cells. Adult T-cell leukemia/lymphoma (ATLL) is developed in HTLV-1-infected T-cells after a long infection period. To examine the mechanism of CADM1 overexpression in ATLL, we first identified that CADM1 is transcriptionally up-regulated by a transcriptional enhancer element through NF-κB signaling pathway. In HTLV-1-infected T-cells, CADM1 expression is dependent on HTLV-1/Tax through activation of canonical and non-canonical NF-κB; however, in ATLL cells with frequent loss of Tax expression, the activation of canonical NF-κB only enhances the CADM1 expression. Along with active mutations in signaling molecules under T-cell recepor (TCR) signaling, degradation of p47, a negative regulator of NF-κB, was essential for activation of canonical NF-κB through stabilization of NEMO (NF-κB essential modulator). The mechanism of p47 degradation is primarily dependent on activation of lysosomal-autophagy and the autophagy is activated in most of the HTLV-infected and ATLL cells, suggesting that the p47 degradation may be a first key molecular event during HTLV-1 infection to T-cells as a connector of two important signaling pathways, NF-κB and autophagy. More... »

PAGES

3491

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41598-019-39424-7

DOI

http://dx.doi.org/10.1038/s41598-019-39424-7

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1112543973

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30837480


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33 schema:description Cell adhesion molecule 1 (CADM1), a member of the immunoglobulin superfamily, is identified as a novel cell surface marker for human T-cell leukemia virus (HTLV-1)-infected T cells. Adult T-cell leukemia/lymphoma (ATLL) is developed in HTLV-1-infected T-cells after a long infection period. To examine the mechanism of CADM1 overexpression in ATLL, we first identified that CADM1 is transcriptionally up-regulated by a transcriptional enhancer element through NF-κB signaling pathway. In HTLV-1-infected T-cells, CADM1 expression is dependent on HTLV-1/Tax through activation of canonical and non-canonical NF-κB; however, in ATLL cells with frequent loss of Tax expression, the activation of canonical NF-κB only enhances the CADM1 expression. Along with active mutations in signaling molecules under T-cell recepor (TCR) signaling, degradation of p47, a negative regulator of NF-κB, was essential for activation of canonical NF-κB through stabilization of NEMO (NF-κB essential modulator). The mechanism of p47 degradation is primarily dependent on activation of lysosomal-autophagy and the autophagy is activated in most of the HTLV-infected and ATLL cells, suggesting that the p47 degradation may be a first key molecular event during HTLV-1 infection to T-cells as a connector of two important signaling pathways, NF-κB and autophagy.
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41 ATLL cells
42 CADM1 expression
43 CADM1 overexpression
44 HTLV
45 HTLV-1 infection
46 HTLV-1/Tax
47 NEMO
48 NF-κB
49 Tax expression
50 activation
51 active mutations
52 adhesion molecule-1
53 adult T
54 autophagy
55 autophagy contributes
56 canonical NF-κB
57 cell adhesion molecule-1
58 cell leukemia virus
59 cell leukemia/lymphoma
60 cell recepor (TCR) signaling
61 cell surface markers
62 cells
63 connectors
64 contributes
65 degradation
66 degradation of p47
67 elements
68 enhancer elements
69 events
70 expression
71 first key molecular event
72 frequent loss
73 immunoglobulin
74 infection
75 infection period
76 key molecular events
77 leukemia virus
78 leukemia/lymphoma
79 long infection period
80 loss
81 lymphoma
82 markers
83 mechanism
84 members
85 molecular events
86 molecule-1
87 molecules
88 mutations
89 negative regulator
90 non-canonical NF-κB
91 novel cell surface marker
92 overexpression
93 p47
94 p47 degradation
95 pathway
96 period
97 recepor (TCR) signaling
98 regulator
99 signaling
100 stabilization
101 stabilization of NEMO
102 surface markers
103 tax
104 transcriptional enhancer element
105 virus
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