These authors contributed equally to this work.
HOTAIR, a prognostic factor in esophageal squamous cell carcinoma, inhibits WIF-1 expression and activates Wnt pathway
Version of Record online: 29 OCT 2013
© 2013 Japanese Cancer Association
Volume 104, Issue 12, pages 1675–1682, December 2013
How to Cite
(Cancer Sci 2013; 104: 1675–1682)
- Issue online: 6 DEC 2013
- Version of Record online: 29 OCT 2013
- Accepted manuscript online: 1 OCT 2013 12:07AM EST
- Manuscript Accepted: 19 SEP 2013
- Manuscript Revised: 9 SEP 2013
- Manuscript Received: 7 JUN 2013
- National Basic Research Program of China. Grant Number: 2011CB504303
- Ministry of Science and Technology of China. Grant Number: 2011ZX09307-001-04
|cas12296-sup-0001-DataS1.docx||Word document||24K||Data S1. Materials and methods.|
Fig. S1. Relative expression of HOTAIR in esophageal squamous cell carcinoma (ESCC) cell lines detected by reverse transcription-polymerase chain reaction (RT-PCR).
Fig. S2. Effects of HOTAIR on the proliferation of KYSE180 and KYSE410 cells.
Fig. S3. HOTAIR induced gene expression changes in KYSE180 cells.
Fig. S4. Overexpression of HOTAIR inhibits WIF-1 promoter activity.
Fig. S5. WIF-1 de-repressed after concomitant EZH2 RNAi in KYSE180-HOTAIR cells.
Fig. S6. HOTAIR-induced migration and invasion were inhibited by exogenous recombinant human WIF-1.
Fig. S7. Concomitant WNT5B RNAi in KYSE180-HOTAIR cells.
|cas12296-sup-0003-TableS1.xlsx||application/msexcel||225K||Table S1. cDNA microarray data in KYSE180-vector cells and KYSE180-HOTAIR cells.|
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