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Cell Lines

Cell Lines

A cell line is a population of cells grown in vitro that can be subcultured over several generations. Normal cells cease to divide after a certain number of cell divisions, a process known as replicative senescence. This number, called the Hayflick limit, was conceptualized by Leonard Hayflick in 1961 when he observed that fetal cells grown in culture could only divide 40-60 times. This limit is due to the shortening of the telomeres during each round of cell division, preventing cell division...

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Updated: Jun 12, 2026

Differentiation of the SH-SY5Y Human Neuroblastoma Cell Line

Differentiation of the SH-SY5Y Human Neuroblastoma Cell Line

Published on: February 17, 2016

Epigenetic alterations differ in phenotypically distinct human neuroblastoma cell lines.

Qiwei Yang¹, Yufeng Tian, Kelly R Ostler

¹Department of Pediatrics, University of Chicago, 900 Ease 57th Street, KCBD Rm, 5100 Chicago, IL 60637, USA.

|June 16, 2010

Summary

Epigenetic changes in neuroblastoma (NB) cells correlate with tumor growth and poor outcomes. Reversing these epigenetic alterations with 5-Aza-dC can inhibit NB tumorigenic properties.

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Last Updated: Jun 12, 2026

Differentiation of the SH-SY5Y Human Neuroblastoma Cell Line

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Neurogenesis Using P19 Embryonal Carcinoma Cells

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Published on: April 27, 2019

Area of Science:

Oncology
Epigenetics
Molecular Biology

Background:

Epigenetic aberrations and CpG island methylator phenotype are linked to poor outcomes in neuroblastoma (NB).
Seven cancer-related genes (THBS-1, CASP8, HIN-1, TIG-1, BLU, SPARC, HIC-1) with known epigenetic changes in adult cancers were investigated for their role in NB phenotype.
These genes are crucial for regulating angiogenesis, tumor growth, and apoptosis.

Purpose of the Study:

To investigate the role of epigenetic alterations in determining neuroblastoma (NB) phenotype.
To analyze the expression and methylation status of seven cancer-related genes in NB cell lines.
To examine the effect of epigenetic modifications on NB cell tumorigenicity.

Main Methods:

Utilized two NB cell lines (LA1-55n and LA1-5s) differing in tumorigenicity.
Performed quantitative RNA expression analysis for seven genes.
Examined promoter methylation status (THBS-1, HIN-1, TIG-1, CASP8) using methylation-specific PCR.
Assessed histone modifications on the THBS-1 promoter via chromatin immunoprecipitation.
Evaluated THBS-1 promoter activity using luciferase assays.
Investigated the impact of 5-Aza-dC on NB cell proliferation, morphology, and soft agar colony formation.

Main Results:

Higher promoter methylation and lower gene expression of THBS-1, HIN-1, TIG-1, and CASP8 were observed in the tumorigenic LA1-55n cells compared to LA1-5s cells.
Repressive histone marks were found on the THBS-1 promoter in LA1-55n cells, while active marks were present in LA1-5s cells.
5-Aza-dC treatment reversed DNA methylation and histone code alterations in the THBS-1 promoter of LA1-55n cells, inhibiting cell morphology changes and soft agar colony formation.

Conclusions:

Epigenetic aberrations significantly contribute to the neuroblastoma (NB) phenotype.
Reversing epigenetic changes using 5-Aza-dC can effectively inhibit the tumorigenic properties of NB cells.
Targeting epigenetic modifications presents a potential therapeutic strategy for neuroblastoma.