|
1
|
Pardal R, Molofsky AV, He S and Morrison
SJ: Stem cell self-renewal and cancer cell proliferation are
regulated by common networks that balance the activation of
proto-oncogenes and tumor suppressors. Cold Spring Harb Symp Quant
Biol. 70:177–185. 2005. View Article : Google Scholar
|
|
2
|
Yasuda SY, Tsuneyoshi N, Sumi T, Hasegawa
K, Tada T, Nakatsuji N and Suemori H: NANOG maintains self-renewal
of primate ES cells in the absence of a feeder layer. Genes Cells.
11:1115–1123. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
3
|
Zhou Q, Chipperfield H, Melton DA and Wong
WH: A gene regulatory network in mouse embryonic stem cells. Proc
Natl Acad Sci USA. 104:16438–16443. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
4
|
Zhang J, Tam WL, Tong GQ, et al: Sall4
modulates embryonic stem cell pluripotency and early embryonic
development by the transcriptional regulation of Pou5f1. Nat Cell
Biol. 8:1114–1123. 2006. View
Article : Google Scholar : PubMed/NCBI
|
|
5
|
Jiang J, Chan YS, Loh YH, et al: A core
Klf circuitry regulates self-renewal of embryonic stem cells. Nat
Cell Biol. 10:353–360. 2008. View
Article : Google Scholar : PubMed/NCBI
|
|
6
|
Okita K, Ichisaka T and Yamanaka S:
Generation of germline- competent induced pluripotent stem cells.
Nature. 448:313–317. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
7
|
Tsubooka N, Ichisaka T, Okita K, Takahashi
K, Nakagawa M and Yamanaka S: Roles of Sall4 in the generation of
pluripotent stem cells from blastocysts and fibroblasts. Genes
Cells. 14:683–694. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
8
|
Yu J, Vodyanik MA, Smuga-Otto K, et al:
Induced pluripotent stem cell lines derived from human somatic
cells. Science. 318:1917–1920. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
9
|
Sakaki-Yumoto M, Kobayashi C, Sato A, et
al: The murine homolog of SALL4, a causative gene in Okihiro
syndrome, is essential for embryonic stem cell proliferation, and
cooperates with Sall1 in anorectal, heart, brain and kidney
development. Development. 133:3005–3013. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
10
|
Jürgens G: Head and tail development of
the Drosophila embryo involves spalt, a novel homeotic gene. EMBO
J. 7:189–196. 1998.
|
|
11
|
Al-Baradie R, Yamada K, St Hilaire C, et
al: Duane radial ray syndrome (Okihiro syndrome) maps to 20q13 and
results from mutations in SALL4, a new member of the SAL family. Am
J Hum Genet. 71:1195–1199. 2002. View
Article : Google Scholar : PubMed/NCBI
|
|
12
|
Kohlhase J, Heinrich M, Liebers M, et al:
Cloning and expression analysis of SALL4, the murine homologue of
the gene mutated in Okihiro syndrome. Cytogenet Genome Res.
98:274–277. 2002. View Article : Google Scholar
|
|
13
|
Ma Y, Cui W, Yang J, et al: SALL4, a novel
oncogene, is constitutively expressed in human acute myeloid
leukemia (AML) and induces AML in transgenic mice. Blood.
108:2726–2735. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
14
|
Cui W, Kong NR, Ma Y, Amin HM, Lai R and
Chai L: Differential expression of the novel oncogene, SALL4, in
lymphoma, plasma cell myeloma, and acute lymphoblastic leukemia.
Mod Pathol. 19:1585–1592. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
15
|
Yang J, Chai L, Gao C, et al: SALL4 is a
key regulator of survival and apoptosis in human leukemic cells.
Blood. 112:805–813. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
16
|
Yang J, Chai L, Liu F, et al: Bmi-1 is a
target gene for SALL4 in hematopoietic and leukemic cells. Proc
Natl Acad Sci USA. 104:10494–10499. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
17
|
Dimri GP, Martinez JL, Jacobs JJ, et al:
The Bmi-1 oncogene induces telomerase activity and immortalizes
human mammary epithelial cells. Cancer Res. 62:4736–4745.
2002.PubMed/NCBI
|
|
18
|
Liu L, Andrews LG and Tollefsbol TO: Loss
of the human polycomb group protein BMI1 promotes cancer-specific
cell death. Oncogene. 25:4370–4375. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
19
|
Kobayashi D, Kuribayashi K, Tanaka M and
Watanabe N: SALL4 is essential for cancer cell proliferation and is
overex-pressed at early clinical stages in breast cancer. Int J
Oncol. 38:933–999. 2011.PubMed/NCBI
|
|
20
|
Kobayashi D, Kuribayashi K, Tanaka M and
Watanabe N: Overexpression of SALL4 in lung cancer and its
importance in cell proliferation. Oncol Rep. 26:965–970.
2011.PubMed/NCBI
|
|
21
|
Jeong HW, Cui W, Yang Y, Lu J, He J, Li A,
Song D, Guo Y, Liu BH and Chai L: SALL4, a stem cell factor,
affects the side population by regulation of the ATP-binding
cassette drug transport genes. PLoS One. 6:e183722011. View Article : Google Scholar : PubMed/NCBI
|
|
22
|
Abou El Hassan MA, Mastenbroek DC,
Gerritsen WR, Giaccone G and Kruyt FA: Overexpression of Bcl2
abrogates chemo- and radiotherapy-induced sensitisation of NCI-H460
non-small-cell lung cancer cells to adenovirus-mediated expression
of full-length TRAIL. Br J Cancer. 91:171–177. 2004. View Article : Google Scholar : PubMed/NCBI
|
|
23
|
Yi H, Cho HJ, Cho SM, Jo K, Park JA, Kim
NH, Amidon GL, Kim JS and Shin HC: Blockade of interleukin-6
receptor suppresses the proliferation of H460 lung cancer stem
cells. Int J Oncol. 41:310–316. 2012.PubMed/NCBI
|
|
24
|
Song L, Rawal B, Nemeth JA and Haura EB:
JAK1 activates STAT3 activity in non-small-cell lung cancer cells
and IL-6 neutralizing antibodies can suppress JAK1-STAT3 signaling.
Mol Cancer Ther. 10:481–494. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
25
|
Bard JD, Gelebart P, Amin HM, Young LC, Ma
Y and Lai R: Signal transducer and activator of transcription 3 is
a transcriptional factor regulating the gene expression of SALL4.
FASEB J. 23:1405–1414. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
26
|
Wu Q, Chen X, Zhang J, et al: Sall4
interacts with Nanog and co-occupies Nanog genomic sites in
embryonic stem cells. J Biol Chem. 281:24090–24094. 2006.
View Article : Google Scholar : PubMed/NCBI
|
