Research Papers:

YdjC chitooligosaccharide deacetylase homolog induces keratin reorganization in lung cancer cells: involvement of interaction between YDJC and CDC16

Eun Ji Kim _, Mi Kyung Park, Hyun Jung Byun, Gyeoung Jin Kang, Lu Yu, Hyun Ji Kim, Jae Gal Shim, Ho Lee and Chang Hoon Lee

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Oncotarget. 2018; 9:22915-22928. https://doi.org/10.18632/oncotarget.25145

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Eun Ji Kim1, Mi Kyung Park2, Hyun Jung Byun1, Gyeoung Jin Kang1, Lu Yu1, Hyun Ji Kim1, Jae Gal Shim2, Ho Lee2 and Chang Hoon Lee1

1College of Pharmacy, Dongguk University-Seoul, 04620, Seoul, South Korea

2National Cancer Center, Goyang, 10408, South Korea

Correspondence to:

Chang Hoon Lee, email: [email protected]

Keywords: YDJC; CDC16; keratin reorganization; migration; invasion

Received: November 22, 2017     Accepted: April 03, 2018     Published: May 01, 2018


Lung cancer is a fatal disease with a high mortality rate. The perinuclear reorganization of keratin 8 (K8) is an important biochemical phenomenon reflecting changes in the physical properties of metastatic cancer. However, there is not much of information about the regulatory molecules involved in phosphorylation and perinuclear reorganization of K8.

In this study, we investigated the role and molecular mechanisms of YdjC chitooligosaccha- ride deacetylase homolog (YDJC) in sphingosylphosphorylcholine (SPC)-induced phosphorylation and reorganization of K8, and migration and invasion (SPC-induced events). SPC induced expression of YDJC in a dose- and time-dependent manner. Gene silencing of YDJC suppressed SPC-induced events. YDJC overexpression induced the SPC-induced events. YDJC deacetylase dominant negative mutant (YDJCD13A) did not induce SPC-induced events. YDJC siRNA reduced ERK activation and overexpression of YDJC induced ERK activation. The siRNA of ERK1 or ERK2 suppressed YDJC-induced phosphorylation and reorganization of K8, and migration and invasion. Co-immunoprecipitation revealed that YDJC binds to CDC16. Interestingly, CDC16 siRNA induced SPC-induced events. Overexpression of CDC16 blocked SPC-induced events. KMPLOT analysis based on public microarray data revealed the poor prognosis of lung cancer patients with high expression of YDJC compared with patients with low expression of YDJC.

The collective results indicate that YDJC is involved in SPC-induced events in A549 lung cancer cells by interacting with CDC16. YDJC overexpression might be involved in the progression of lung cancer. These results also suggest that suppression of YDJC or boosting of CDC16 interaction with YDJC might be a novel way to prevent progression of lung cancer.

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