American Association for Cancer Research
00085472can122377-sup-fig1-4.pdf (161.56 kB)

Supplementary Figures 1 - 4 from ALX1 Induces Snail Expression to Promote Epithelial-to-Mesenchymal Transition and Invasion of Ovarian Cancer Cells

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journal contribution
posted on 2023-03-30, 22:00 authored by Hong Yuan, Hiroaki Kajiyama, Satoko Ito, Nobuhisa Yoshikawa, Toshinori Hyodo, Eri Asano, Hitoki Hasegawa, Masao Maeda, Kiyosumi Shibata, Michinari Hamaguchi, Fumitaka Kikkawa, Takeshi Senga

PDF file - 161K, Cell lines subjected to in vitro invasion assay and soft agar colony formation assay (S1); SKOV3 cells that constitutively expressed GFP-ALX1 or siRNA-resistant GFP-ALX1 (ALX1-Res#2) was established by retrovirus infection (S2); SKOV3 cells were transfected with Ctrl or ALX1 siRNAs and cell growth was evaluated by MTT assay (S3); ALX1 induces EMT in NOS3 cells (S4)



Ovarian cancer is a highly invasive and metastatic disease with a poor prognosis if diagnosed at an advanced stage, which is often the case. Recent studies argue that ovarian cancer cells that have undergone epithelial-to-mesenchymal transition (EMT) acquire aggressive malignant properties, but the relevant molecular mechanisms in this setting are not well-understood. Here, we report findings from an siRNA screen that identified the homeobox transcription factor ALX1 as a novel regulator of EMT. RNA interference–mediated attenuation of ALX1 expression restored E-cadherin expression and cell–cell junction formation in ovarian cancer cells, suppressing cell invasion, anchorage-independent growth, and tumor formation. Conversely, enforced expression of ALX1 in ovarian cancer cells or nontumorigenic epithelial cells induced EMT. We found that ALX1 upregulated expression of the key EMT regulator Snail (SNAI1) and that it mediated EMT activation and cell invasion by ALX1. Our results define the ALX1/Snail axis as a novel EMT pathway that mediates cancer invasion. Cancer Res; 73(5); 1581–90. ©2012 AACR.