Rac1-dependent lamellipodial motility in prostate cancer PC-3 cells revealed by optogenetic control of Rac1 activity

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Rac1-dependent lamellipodial motility in prostate cancer PC-3 cells revealed by optogenetic control of Rac1 activity

Persistent ID (NDL): info:ndljp/pid/10224393

Material type: 博士論文

Author: 加藤, 琢磨

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Publication date: 2014-12-24

Material Format: Digital

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Name of awarding university/degree: 香川大学,博士（医学）

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Note (General)：: AbstractThe lamellipodium, an essential structure for cell migration, plays an important role in the invasion and metastasis of cancer cells. Although...

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Material Type: 博士論文
Title: Rac1-dependent lamellipodial motility in prostate cancer PC-3 cells revealed by optogenetic control of Rac1 activity
Author/Editor: 加藤, 琢磨
Author Heading: 加藤, 琢磨
Publication Date: 2014-12-24
Publication Date (W3CDTF): 2014-12-24
Degree grantor/type: 香川大学
Date Granted: 2014-12-24
Date Granted (W3CDTF): 2014-12-24
Dissertation Number: 甲第598号
Degree Type: 博士（医学）
Conferring No. (Dissertation): 甲第598号
Text Language Code: eng
Alias of Author: Kato, Takuma
Target Audience: 一般
Note (General): AbstractThe lamellipodium, an essential structure for cell migration, plays an important role in the invasion and metastasis of cancer cells. Although Rac1 recognized as a key player in the formation of lamellipodia, the molecular mechanisms underlying lamellipodial motility are not fully understood. Optogenetic technology enabled us to spatiotemporally control the activity of photoactivatable Rac1 (PA-Rac1) in living cells. Using this system, we revealed the role of phosphatidylinositol 3-kinase (PI3K) in Rac1-dependent lamellipodial motility in PC-3 prostate cancer cells. Through local blue laser irradiation of PA-Rac1-expressing cells, lamellipodial motility was reversibly induced. First, outward extension of a lamellipodium parallel to the substratum was observed. The extended lamellipodium then showed ruffling activity at the periphery. Notably, PI(3,4,5)P3 and WAVE2 were localized in the extending lamellipodium in a PI3K-dependent manner. We confirmed that the inhibition of PI3K activity greatly suppressed lamellipodial extension, while the ruffling activity was less affected. These results suggest that Rac1-induced lamellipodial motility consists of two distinct activities, PI3K-dependent outward extension and PI3K-independent ruffling.
DOI: info:doi/10.1371/journal.pone.0097749
https://doi.org/info:doi/10.1371/journal.pone.0097749
Persistent ID (NDL): info:ndljp/pid/10224393
https://dl.ndl.go.jp/pid/10224393
Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
https://dl.ndl.go.jp/collections/A00014
Acquisition Basis: 博士論文（自動収集）
Date Accepted (W3CDTF): 2016-12-01T22:39:34+09:00
Date Created (W3CDTF): 2020-10-27
Format (IMT): PDF
Access Restrictions: 国立国会図書館内限定公開
Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
Availability of remote photoduplication service: 可
Original Material (URI): https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-25861427/
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-24659087/
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23390039/
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-26860136/
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-24890154/
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-25860142/
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-24390369/
Periodical Title (URI): https://kagawa-u.repo.nii.ac.jp/records/230
Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション
https://dl.ndl.go.jp