Tumor growth rate of pancreatic serous cystadenomas: Endosonographic follow-up with volume measurement to predict cyst enlargement

Salom, Federico; Piedra, William; Burgos, Herbert

doi:10.1016/j.pan.2018.11.007

Cited by 5 publications

(1 citation statement)

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“…HL-60 SATB1 -shRNA1 and HL-60 control cells (1 × 10 7 ) were injected subcutaneously in SATB1 -shRNA1 and control mice, respectively. Tumor size was measured everyday and tumor volume was calculated by the formula: tumor volume [mm 3 ] = (length [mm]) × (width [mm]) 2 × 0.5 [26].…”

Section: Methodsmentioning

confidence: 99%

Decreased SATB1 expression promotes AML cell proliferation through NF-κB activation

Luo

et al. 2019

Cancer Cell Int

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Background Special AT-rich sequence-binding protein 1 (SATB1) is a chromatin-remodeling protein that regulates gene expressions in different types of cancer. Up-regulation of SATB1 is linked with progression of tumors. Our previous study showed that SATB1 expression was decreased in T cell leukemia/lymphoma. The contrary roles of SATB1 in solid organ tumors and hematology malignancy may provide hints to study the function of SATB1. Methods To characterize SATB1 mRNA and protein expression in acute myeloid leukemia (AML), we performed qRT-PCR and Western blot on bone marrow mononuclear cells from 52 newly diagnosed AML patients. Stable HL-60 cell lines with knockdown of SATB1 by shRNAs sequences (HL-60 SATB1-shRNA1 and HL-60 SATB1-shRNA2) were established. Cell proliferation, cell cycle and cell invasiveness were analyzed. Murine model was established using HL-60 SATB1-shRNAs treated nude mice and tumorigenicity was compared to study the role of SATB1 in vivo. Global gene expression profiles were analyzed in HL-60 cells with SATB1 knockdown to investigate the mechanisms underlying the regulation of AML cell growth by SATB1. Results We found that SATB1 expression was significantly decreased in patients with AML compared to normal control, and was increased after complete remission of AML. Knockdown of SATB1 enhanced the proliferation of HL-60 cells and accelerated S phase entry in vitro, and promoted the tumor growth in vivo. Global gene expression profiles were analyzed in HL-60 cells with SATB1 knockdown and the differentially expressed genes were involved in NF-κB, MAPK and PI3 K/Akt signaling pathways. Nuclear NF-κB p65 levels were significantly increased in SATB1 depleted HL-60 cells. Conclusions Decreased SATB1 expression promotes AML cell proliferation through NF-κB activation. SATB1 could be a predictor for better response to treatment in AML.

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Section: Methodsmentioning

confidence: 99%