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These data indicate that aberrantly expressed SALL4 in human choriocarcinoma cells may promote cell proliferation via beta-catenin/c-Myc pathway
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SALL4 was significantly upregulated in glioma tissues and cell lines, and an inverse correlation between miR-98 and SALL4 expression in glioma tissues was identified.
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TNFSF13, SPATC1L, SLC22A25 and SALL4 may thus be novel susceptibility loci for atrial fibrillation in the Japanese population
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Study showed significantly high expression of SALL4 mRNA in glioma specimens as compared to non-tumor samples using RT-PCR. Blocking SALL4 using SALL4-siRNA decreased proliferation of U87 and U251 cells, which was reversed by the addition of PTEN inhibitor phen (bpv). Furthermore, marked increase in PTEN mRNA and protein levels was seen in cells treated with siRNA-SALL4.
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SALL4 is a promising prognostic biomarker for cancer, and is appropriate for the assessment of cancer prognosis in the Chinese people.
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Our experimental data indicated that over expression of SALL4 was found in CRC and low expression of SALL4 was connected with high survival rate after surgery. Thus our study suggested that SALL4 could serve as a potential diagnostic and prognostic marker of CRC.
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SALL4 is a target gene of miR-181b in glioma.SALL4 is upregulated in glioma.
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SALL4 is a target gene of mir-98 in non-small cell lung cancer cells.
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miR-98 plays a suppressive role in the proliferation, migration, invasion and EMT of HCC cells, partly at least, via directly inhibition of SALL4.
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SALL4 immunopositivity is not a prognostic factor in Combined hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC) (cHCC-CC); however, it is associated with alpha-fetoprotein, glypican 3 and EpCAM immunopositivity, indicating the mechanism of carcinogenesis.
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these data suggest that Bmi-1 could serve as a novel prognostic biomarker in pediatric primary acute lymphoblastic leukemia (ALL)and may be partially regulated by Sall4a. Our study also showed that Bmi-1 could serve as a new therapeutic target for the treatment of pediatric ALL.
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SALL4 overexpression is associated with neoplasms.
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Findings indicate that long-term exposure to IM results in dysregulation of stem cell renewal-regulatory Hippo (MST1/2)/YAP signaling, and that inhibition of miR-181a using a microRNA sponge inhibitor resulted in decreased transcription of SOX2 and SALL4.
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Study showed that SALL4 was overexpressed in a majority of human esophageal squamous cell carcinoma (ESCC) tissues and that aberrantly activated SALL4 may contribute to esophageal tumorigenesis by promoting malignant proliferation and inhibiting cell apoptosis, regulating esophageal squamous cell migration, invasion and cell cycle.
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Data show that SALL4 promotes the expression of Glut1 and open chromatin through a HP1alpha-dependent mechanism.
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Our report is the first description of structural eye defects associated with two missense variants in SALL4 inherited in trans; the absence of reported findings in both parents suggests that both sequence variants are hypomorphic mutations and that both are needed for the ocular phenotype.
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our study showed that SALL4 plays an important role in regulating the proliferation, migration, and invasion of osteosarcoma cells.
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The SALL4 - integrin alpha6 - integrin beta1 network promotes cell migration for metastasis via activation of focal adhesion dynamics in basal-like breast cancer cells.
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Coexpression of SALL4 with HDAC1 and/or HDAC2 was associated with PTEN underexpression and a poor prognosis in hepatocellular carcinoma.
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SALL4 has a negative impact in DNA damage repair, and support the model of dual functional properties of SALL4 in leukemogenesis through inhibiting DNA damage repair and promoting cell survival.
