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Authors demonstrated that TSSC3 was an independent prognostic marker for overall survival in osteosarcoma, and positive ATG5 expression associated with positive TSSC3 expression suggested a favorable prognosis for patients. Then, we showed that TSSC3 overexpression enhanced autophagy via inactivating the Src-mediated PI3K/Akt/mTOR pathway in osteosarcoma.
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RanBP9/TSSC3 complex cooperatively suppress metastasis via downregulation of Src-dependent Akt pathway to expedite mitochondrial-associated anoikis.
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PHLDA2 plays an important role in the occurrence and development of pregnancy complications by promoting trophoblast apoptosis and suppressing cell invasion.
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TSSC3 was a prognostic marker in osteosarcoma.
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TSSC3 downregulation promotes the Epithelial to mesenchymal transition (EMT) of osteosarcoma cells by regulating EMT markers via a signal transduction pathway that involves Snail, Wnt-beta-catenin/TCF, and GSK-3beta
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Placental PHLDA2 expression was significantly 2.3 fold higher in reduced fetal movements pregnancies resulting in delivery of a growth restricted compared with a normal birth weight infant.
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PHLDA2 may promote the occurrence/development of preeclampsia by inhibiting proliferation/migration/invasion of trophoblasts.
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The gene expression pattern of CDKN1C, H19, IGF2, KCNQ1 and PHLDA2 genes was evaluated using RT-PCR.
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elevated expression in placenta of growth restricted pregnancies [review]
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results suggest upregulated pleckstrin homology-like domain family A member 2 (PHLDA2) in placenta of monozygotic twins may be associated with the pathogenesis of singleton intrauterine growth restriction
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TSSC3 overexpression suppressed osteosarcoma cell growth and increased apoptosis through caspase-3 upregulation, suggesting that TSSC3 may play a pro-apoptosis role to maintain the normal balance of growth
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TSSC3 inhibits osteosarcoma tumorigenicity through reducing stemness and promoting apoptosis of tumor inducing cells
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A luciferase reporter assay was used to identify in the PHLDA2 promoter a 15 bp repeat sequence variant that significantly reduces PHLDA2-promoter efficiency. Maternal inheritance of the variant resulted in a significant increase in birth weight.
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The results suggest that placental PHLDA2 may provide a biomarker for suboptimal skeletal growth in pregnancies uncomplicated by overt fetal growth restriction.
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TSSC3 has a potent tumor suppressor role in osteosarcoma, probably by inhibition of growth and induction of apoptosis via the mitochondrial apoptosis pathway.
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PHLDA2 is a target gene of the BACH1 transcription factor according to ChIP-seq analysis in HEK 293 cells.
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Expression levels of PHLDA2 gene were upregulated in the first trimester pregnancy
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PHLDA2 gene is imprinted, with preferential expression from the maternal allele in placenta and liver.
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Transcripts of TSSC3 could not be detected in human oocytes and preimplantation embryos.
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Exposure of trophoblasts to hypoxia in vitro markedly reduced the expression of PHLDA2.