フルテキストURL J_Cell_Biochem_116_10_2146.pdf
著者 Eguchi , Taka| Prince, Thomas| Wegiel, Barbara| Calderwood, Stuart K.|
抄録 Myeloid zinc finger 1 (MZF1) belongs to the SCAN-Zinc Finger (SCAN-ZF) transcription factor family that has recently been implicated in a number of types of cancer. Although the initial studies concentrated on the role of MZF1 in myeloid differentiation and leukemia, the factor now appears to be involved in the etiology of major solid tumors such as lung, cervical, breast, and colorectal cancer. Here we discuss the regulation of MZF1 that mediated its recruitment and activation in cancer, concentrating on posttranslational modification by phosphorylation, and sumoylation, formation of promyelocytic leukemia nuclear bodies and its association with co-activators and co-repressors.
キーワード CANCER FINGER-1 INVASION MYELOID NUCLEAR BODY SUMO ZINC
発行日 2015-04-21
出版物タイトル Journal of cellular biochemistry
116巻
10号
出版者 Wiley
開始ページ 2146
終了ページ 2154
ISSN 0730-2312
NCID AA1052210X
資料タイプ 学術雑誌論文
言語 Japanese
OAI-PMH Set 岡山大学
論文のバージョン author
PubMed ID 25903835
DOI 10.1002/jcb.25203
Web of Sience KeyUT 000359809400004
関連URL isVersionOf https://doi.org/10.1002/jcb.25203
著者 Okusha, Yuka| Eguchi, Takanori| Sogawa, Chiharu| Okui, Tatsuo| Nakano, Keisuke| Okamoto, Kuniaki| Kozaki, Ken‐Ichi|
抄録 Members of matrix metalloproteinase (MMP) family promote cancer cell migration, invasion, and metastasis through alteration of the tumor milieu, intracellular signaling pathways, and transcription. We examined gene expression signatures of colon adenocarcinoma cell lines with different metastatic potentials and found that rapidly metastatic cells powerfully expressed genes encoding MMP3 and MMP9. The non-proteolytic PEX isoform and proteolytic isoforms of MMPs were significantly expressed in the metastatic cells in vitro. Knockdown of MMP3 attenuated cancer cell migration and invasion in vitro and lung metastasis in vivo. Profound nuclear localization of MMP3/PEX was found in tumor-stroma marginal area. In contrast, MMP9 was localized in central area of subcutaneous tumors. Overexpression of the PEX isoform of MMP3 promoted proliferation and migration of the rapidly metastatic cells in vitro. Taken together, the non-proteolytic PEX isoform of MMPs locating in cell nuclei involves proliferation, migration, and subsequent metastasis of aggressive adenocarcinoma cells.
キーワード PEX domain cancer metastasis non-proteolytic MMP nuclear MMP tumor stroma
備考 This fulltext will be available in May 2019
発行日 2018-05-15
出版物タイトル Journal of Cellular Biochemistry
出版者 Wiley
ISSN 1097-4644
NCID AA1052210X
資料タイプ 学術雑誌論文
言語 English
OAI-PMH Set 岡山大学
論文のバージョン author
PubMed ID 29761931
DOI 10.1002/jcb.27040
関連URL isVersionOf https://doi.org/10.1002/jcb.27040
フルテキストURL J_Cell_Biochem_118_1_43.pdf
著者 Eguchi, Takanori| Calderwood, Stuart K.| Takigawa, Masaharu| Kubota, Satoshi| Kozaki, Ken‐ichi|
抄録 Matrix metalloproteinases (MMPs) are crucial factors in tumor progression, inflammatory/immune responses and tissue development/regeneration. Of note, it has been known that MMPs promote genome instability, epithelial-mesenchymal transition, invasion, and metastasis in tumor progression. We previously reported that human MMP3 could translocate into cellular nuclei and control transcription in human chondrosarcoma-derived cells and in articular cartilage (Eguchi et al. [2008] Mol Cell Biol 28(7):2391-2413); however, further transcriptional target genes and cofactors of intranuclear MMP3 have not been uncovered. In this paper, we used transcriptomics analysis in order to examine novel transcriptional target genes regulated by intracellular MMP3. We found that mRNA levels of HSP family members (HSP70B', HSP72, HSP40/DNAJ, and HSP20/CRYAB) are upregulated by the intracellular MMP3 overload. Bioinformatic analysis predicted several transcription factors that possibly interact with MMP3. Among these factors, heat shock factor 1 (HSF1) cooperated with the MMP3 to activate the HSP70B' gene promoter in reporter gene assays, while a dominant negative HSF1 blocked the role for MMP3 in the trans-activation. The hemopexin-like repeat (PEX) domain of the human MMP3 was essential for transcriptional induction of the HSP70B' gene. In addition, chromobox proteins CBX5/HP1α and CBX3/HP1γ cooperated with the PEX domain in induction of HSP70B' mRNA. Taken together, this study newly clarified that intracellular MMP3 cooperate with CBXs/HP1s in transcriptional promotion of HSP genes.
キーワード CBXs CHROMOBOX PROTEINS HEAT SHOCK FACTOR 1 HEAT SHOCK PROTEINS HETEROCHROMATIN PROTEINS HP1 HSF1 HSPs MATRIX METALLOPROTEINASE MMP3 TRANSCRIPTION
発行日 2016-05-21
出版物タイトル Journal of Cellular Biochemistry
118巻
1号
出版者 Wiley
開始ページ 43
終了ページ 51
ISSN 07302312
NCID AA1052210X
資料タイプ 学術雑誌論文
言語 English
OAI-PMH Set 岡山大学
論文のバージョン author
PubMed ID 27206651
DOI 10.1002/jcb.25607
Web of Sience KeyUT 000387809300005
関連URL isVersionOf https://doi.org/10.1002/jcb.25607
著者 Ono, Kisho| Eguchi , Takanori| Sogawa, Chiharu| Calderwood, Stuart K.| Futagawa, Junya| Kasai, Tomonari| Seno, Masaharu| Okamoto, Kuniaki| Sasaki, Akira| Kozaki, Ken‐ichi|
抄録 Cancer cells often secrete extracellular vesicles (EVs) that carry heat shock proteins (HSPs) with roles in tumor progression. Oral squamous cell carcinoma (OSCC) belongs to head and neck cancers (HNC) whose lymph-node-metastases often lead to poor prognosis. We have examined the EV proteome of OSCC cells and found abundant secretion of HSP90-enriched EVs in lymph-node-metastatic OSCC cells. Double knockdown of HSP90α and HSP90β, using small interfering RNA significantly reduced the survival of the metastatic OSCC cells, although single knockdown of each HSP90 was ineffective. Elevated expression of these HSP90 family members was found to correlate with poor prognosis of HNC cases. Thus, elevated HSP90 levels in secreted vesicles are potential prognostic biomarkers and therapeutic targets in metastatic OSCC.
キーワード EV proteomics exosome extracellular vesicle heat shock proteins lymph-node-metastatic oral cancer molecular chaperone
備考 This fulltext will be available in May 2019
発行日 2018-05-16
出版物タイトル Journal of Cellular Biochemistry
出版者 Wiley
ISSN 07302312
NCID AA1052210X
資料タイプ 学術雑誌論文
言語 English
OAI-PMH Set 岡山大学
論文のバージョン author
PubMed ID 29768689
DOI 10.1002/jcb.27039
関連URL isVersionOf https://doi.org/10.1002/jcb.27039
フルテキストURL K0005478_other1.pdf
著者 Matsuzono, Kosuke| Ikeda, Yoshio| Liu, Wentao| Kurata, Tomoko| Deguchi, Shoko| Deguchi, Kentaro| Abe, Koji|
キーワード Prion disease Novelgene mutation 2bp deletion in codon 178 stopcodon at codon 195 Sensoryneuropathy HSAN Pan-autonomicfailure Familial case
備考 岡山大学審査学位副論文
発行日 2013-05
出版物タイトル European journal of neurology
20巻
5号
出版者 Wiley
開始ページ e67
終了ページ e69
ISSN 1351-5101
NCID AA11015934
資料タイプ 学術雑誌論文
言語 English
OAI-PMH Set 岡山大学
著作権者 https://creativecommons.org/licenses/by-nc-sa/4.0/deed.ja
論文のバージョン author
PubMed ID 23577609
Web of Sience KeyUT 000317609800003
関連URL https://doi.org/10.1111/ene.12089 http://ousar.lib.okayama-u.ac.jp/55031