Down-regulation of DPH2L gene during cellular differentiation /apoptosis

Use of mRNA differential display

Guizhong Liu, Nicoletta Ferrari, Giovanni Levi, Min Wu

Research output: Contribution to journalArticle

Abstract

To characterize the genes associated with differentiation/apoptosis induced by all-trons retinoic acid (ATRA) in human lung cancer cells, mRNA differential display was employed. Six cDNA fragments have been isolated, and one of them corresponds to a sequence-known gene DPH2L with unknown function, which was first isolated from the critical region of deletion on chromosome 17p13.3 in human ovarian carcinoma, and regarded as a candidate tumor suppressor gene. Results show that DPH2L is a wide expressed gene, and has another major transcript besides the previously reported 2.3 kb transcript. It is proved that the DPH2L gene is down-regulated during differentiation or apoptosis in several kinds of cancer cells induced by all-trans retinoic acid and N-(4-hydroxyphenyl) retinamide (4HPR). This may suggest that DPH2L does not play a role as a tumor suppressor gene, on the contrary, its down-regulation may be functionally involved in the transition from cell growth to differentiation or apoptosis.

Original languageEnglish
Pages (from-to)496-503
Number of pages8
JournalChinese Science Bulletin
Volume44
Issue number6
Publication statusPublished - Mar 1999

Fingerprint

Gene Expression Profiling
Down-Regulation
Apoptosis
Tretinoin
Tumor Suppressor Genes
Genes
Fenretinide
Chromosome Deletion
Lung Neoplasms
Complementary DNA
Carcinoma
Growth
Neoplasms

Keywords

  • Apoptosis
  • Cell differentiation
  • mRNA differential display
  • Retinoic acids
  • Tumor suppressor gene

ASJC Scopus subject areas

  • General

Cite this

Down-regulation of DPH2L gene during cellular differentiation /apoptosis : Use of mRNA differential display. / Liu, Guizhong; Ferrari, Nicoletta; Levi, Giovanni; Wu, Min.

In: Chinese Science Bulletin, Vol. 44, No. 6, 03.1999, p. 496-503.

Research output: Contribution to journalArticle

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