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Information Journal Paper

Title

LRSAM1 DEPLETION AFFECTS NEUROBLASTOMA SH-SY5Y CELL GROWTH AND MORPHOLOGY: THE LRSAM1 C.2047-1G>A LOSS-OF-FUNCTION VARIANT FAILS TO RESCUE THE PHENOTYPE

Pages

  340-347

Abstract

 Objective: Deleterious variants in LRSAM1, a RING finger ubiquitin ligase which is also known as TSG101-associated ligase (TAL), have recently been associated with Charcot-Marie-Tooth disease type 2P (CMT2P). The mechanism by which mutant LRSAM1 contributes to the development of neuropathy is currently unclear. The aim of this study was to induce LRSAM1 deficiency in a neuronal cell model, observe its effect on CELL GROWTH and morphology and attempt to rescue the phenotype with ancestral and mutantLRSAM1 transfections.Materials and Methods: In this experimental study, we investigated the effect of LRSAM1 downregulation on neuroblastoma SH-SY5Y cells by siRNA technology where cells were transfected with siRNA againstLRSAM1. The effects on the expression levels of TSG101, the only currently known LRSAM1 interacting molecule, were also examined. An equal dosage of ancestral or mutantLRSAM1 construct was transfected in LRSAM1 -downregulated cells to investigate its effect on the phenotype of the cells and whether cell proliferation and morphology could be rescued.Results: A significant reduction in TSG101 levels was observed with the downregulation of LRSAM1. In addition, LRSAM1knockdown significantly decreased the growth rate of SH-SY5Y cells which is caused by a decrease in cell proliferation. An effect on cell morphology was also observed. Furthermore, we overexpressed the ancestral and the c.2047-1G>A mutantLRSAM1 in knocked down cells. Ancestral LRSAM1 recovered cell proliferation and partly the morphology, however, the c.2047-1G>A mutant did not recover cell proliferation and further aggravated the observed changes in cell morphology.Conclusion: Our findings suggest that depletion of LRSAM1 affects neuroblastoma cells growth and morphology and that overexpression of the c.2047-1G>A mutant form, unlike the ancestralLRSAM1, fails to rescue the phenotype.

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    APA: Copy

    MINAIDOU, ANNA, NICOLAOU, PASCHALIS, & CHRISTODOULOU, KYPROULA. (2018). LRSAM1 DEPLETION AFFECTS NEUROBLASTOMA SH-SY5Y CELL GROWTH AND MORPHOLOGY: THE LRSAM1 C.2047-1G>A LOSS-OF-FUNCTION VARIANT FAILS TO RESCUE THE PHENOTYPE. CELL JOURNAL (YAKHTEH), 20(3), 340-347. SID. https://sid.ir/paper/706527/en

    Vancouver: Copy

    MINAIDOU ANNA, NICOLAOU PASCHALIS, CHRISTODOULOU KYPROULA. LRSAM1 DEPLETION AFFECTS NEUROBLASTOMA SH-SY5Y CELL GROWTH AND MORPHOLOGY: THE LRSAM1 C.2047-1G>A LOSS-OF-FUNCTION VARIANT FAILS TO RESCUE THE PHENOTYPE. CELL JOURNAL (YAKHTEH)[Internet]. 2018;20(3):340-347. Available from: https://sid.ir/paper/706527/en

    IEEE: Copy

    ANNA MINAIDOU, PASCHALIS NICOLAOU, and KYPROULA CHRISTODOULOU, “LRSAM1 DEPLETION AFFECTS NEUROBLASTOMA SH-SY5Y CELL GROWTH AND MORPHOLOGY: THE LRSAM1 C.2047-1G>A LOSS-OF-FUNCTION VARIANT FAILS TO RESCUE THE PHENOTYPE,” CELL JOURNAL (YAKHTEH), vol. 20, no. 3, pp. 340–347, 2018, [Online]. Available: https://sid.ir/paper/706527/en

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