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KIAA1199 promotes migration and invasion by Wnt/β-catenin pathway and MMPs mediated EMT progression and serves as a poor prognosis marker in gastric cancer.

Abstract KIAA1199 was upregulated in diverse cancers, but the association of KIAA1199 with gastric cancer (GC), the biological role of KIAA1199 in GC cells and the related molecular mechanisms remain to be elucidated.
PMID
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Mayor MeshTerms
Keywords
Journal Title plos one
Publication Year Start




PMID- 28422983
OWN - NLM
STAT- In-Process
DA  - 20170419
LR  - 20170419
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 4
DP  - 2017
TI  - KIAA1199 promotes migration and invasion by Wnt/beta-catenin pathway and MMPs
      mediated EMT progression and serves as a poor prognosis marker in gastric cancer.
PG  - e0175058
LID - 10.1371/journal.pone.0175058 [doi]
AB  - BACKGROUND: KIAA1199 was upregulated in diverse cancers, but the association of
      KIAA1199 with gastric cancer (GC), the biological role of KIAA1199 in GC cells
      and the related molecular mechanisms remain to be elucidated. METHODS: KIAA1199
      expression was analysed by reverse transcription-polymerase chain reaction assay 
      (RT-PCR) and immunohistochemistry (IHC) in GC patient tissue. The small hairpin
      RNA (shRNA) was applied for the knockdown of endogenous KIAA1199 in NCI-N87 and
      AGS cells. MTT, colony formation, scratch wounding migration, transwell chamber
      migration and invasion assays were employed respectively to investigate the role 
      of KIAA1199 in GC cells. The potential signaling pathway of KIAA1199 induced
      migration and invasion was detected. RESULTS: KIAA1199 was upregulated in GC
      tissue and was an essential independent marker for poor prognosis. Knockdown
      KIAA1199 suppressed the proliferation, migration and invasion in GC cells.
      KIAA1199 stimulated the Wnt/beta-catenin signaling pathway and the enzymatic
      activity of matrix metalloproteinase (MMP) family members and thus accelerated
      the epithelial-to-mesenchymal transition (EMT) progression in GC cells.
      CONCLUSION: These findings demonstrated that KIAA1199 was upregulated in GC
      tissue and associated with worse clinical outcomes in GC, and KIAA1199 acted as
      an oncogene by promoting migration and invasion through the enhancement of
      Wnt/beta-catenin signaling pathway and MMPs mediated EMT progression in GC cells.
FAU - Jia, Shuqin
AU  - Jia S
AD  - Laboratory of Surgery, the Affiliated Hospital of Inner Mongolia Medical
      University, Hohhot, China.
AD  - Center for Molecular Diagnosis, Key Laboratory of Carcinogenesis and
      Translational Research (Ministry of Education), Peking University Cancer Hospital
      & Institute, Beijing, China.
FAU - Qu, Tingting
AU  - Qu T
AD  - Center for Molecular Diagnosis, Key Laboratory of Carcinogenesis and
      Translational Research (Ministry of Education), Peking University Cancer Hospital
      & Institute, Beijing, China.
FAU - Wang, Xiaohong
AU  - Wang X
AD  - Tissue Bank, Key Laboratory of Carcinogenesis and Translational Research
      (Ministry of Education), Peking University Cancer Hospital & Institute, Beijing, 
      China.
FAU - Feng, Mengmeng
AU  - Feng M
AD  - Laboratory of Surgery, the Affiliated Hospital of Inner Mongolia Medical
      University, Hohhot, China.
FAU - Yang, Yang
AU  - Yang Y
AD  - Laboratory of Surgery, the Affiliated Hospital of Inner Mongolia Medical
      University, Hohhot, China.
FAU - Feng, Xuemin
AU  - Feng X
AD  - Laboratory of Surgery, the Affiliated Hospital of Inner Mongolia Medical
      University, Hohhot, China.
FAU - Ma, Ruiting
AU  - Ma R
AD  - Laboratory of Surgery, the Affiliated Hospital of Inner Mongolia Medical
      University, Hohhot, China.
FAU - Li, Wenmei
AU  - Li W
AD  - Center for Molecular Diagnosis, Key Laboratory of Carcinogenesis and
      Translational Research (Ministry of Education), Peking University Cancer Hospital
      & Institute, Beijing, China.
FAU - Hu, Ying
AU  - Hu Y
AD  - Tissue Bank, Key Laboratory of Carcinogenesis and Translational Research
      (Ministry of Education), Peking University Cancer Hospital & Institute, Beijing, 
      China.
FAU - Feng, Yi
AU  - Feng Y
AD  - Center for Molecular Diagnosis, Key Laboratory of Carcinogenesis and
      Translational Research (Ministry of Education), Peking University Cancer Hospital
      & Institute, Beijing, China.
FAU - Ji, Ke
AU  - Ji K
AD  - Department of Gastrointestinal Surgery, Key Laboratory of Carcinogenesis and
      Translational Research (Ministry of Education), Peking University Cancer Hospital
      & Institute, Beijing, China.
FAU - Li, Ziyu
AU  - Li Z
AD  - Department of Gastrointestinal Surgery, Key Laboratory of Carcinogenesis and
      Translational Research (Ministry of Education), Peking University Cancer Hospital
      & Institute, Beijing, China.
FAU - Jiang, Wenguo
AU  - Jiang W
AD  - Cardiff China Medical Research Collaborative, Cardiff University School of
      Medicine, Cardiff, United Kingdom.
FAU - Ji, Jiafu
AU  - Ji J
AD  - Department of Gastrointestinal Surgery, Key Laboratory of Carcinogenesis and
      Translational Research (Ministry of Education), Peking University Cancer Hospital
      & Institute, Beijing, China.
LA  - eng
PT  - Journal Article
DEP - 20170419
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
EDAT- 2017/04/20 06:00
MHDA- 2017/04/20 06:00
CRDT- 2017/04/20 06:00
PHST- 2016/12/13 [received]
PHST- 2017/03/20 [accepted]
AID - 10.1371/journal.pone.0175058 [doi]
AID - PONE-D-16-49325 [pii]
PST - epublish
SO  - PLoS One. 2017 Apr 19;12(4):e0175058. doi: 10.1371/journal.pone.0175058.
      eCollection 2017.

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