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An 80 Kb P1 clone from chromosome 3p21.3 suppresses tumor growth in vivo

M C Todd1, R H Xiang, D K Garcia

  • 1Department of Cellular and Structural Biology, The University of Health Science Center, San Antonio, Texas 78284-7762, USA.

Oncogene
|December 5, 1996
PubMed

Insights

Tumor suppressor genes on chromosome 3p are implicated in small cell lung cancer (SCLC). Researchers identified an 80 kb region within a specific P1 clone that suppresses tumor growth in mouse models.

Area of Science:

  • Genetics
  • Oncology
  • Molecular Biology

Background:

  • Allelic loss on chromosome 3p is frequent in small cell lung cancer (SCLC) and other tumors, suggesting tumor suppressor genes in these regions.
  • Specific SCLC cell lines (NCI H740, GLC20) exhibit homozygous deletions at 3p21.3, overlapping with a tumor-suppressive DNA fragment in a hybrid cell line (HA(3)BB9F).

Purpose of the Study:

  • To identify and functionally characterize tumor suppressor genes within the commonly deleted 3p21.3 region in SCLC.
  • To narrow down the location of a potential tumor suppressor locus responsible for suppressing tumorigenicity.

Main Methods:

  • Isolation of human DNA sequences from the tumor-suppressive hybrid cell line HA(3)BB9F using inter Alu PCR.
  • Development of a 450 Kb P1 contig common to SCLC deletions and the hybrid DNA.
  • Functional assay of individual P1 clones for tumor suppressor activity by transfecting mouse fibrosarcoma cells (A9) and evaluating tumorigenicity in nude mice.

Main Results:

  • A 450 Kb P1 contig was constructed, representing the overlapping region of homozygous deletions in SCLC lines and the tumor-suppressive hybrid.
  • One P1 clone, when introduced into A9 cells, successfully suppressed tumor formation in athymic nude mice.
  • Two other P1 clones from the same contig did not exhibit tumor suppressive activity.

Conclusions:

  • The study functionally delimits a tumor suppressor locus to an 80 kb region within a specific P1 clone at chromosome 3p21.3.
  • This finding provides a refined target for further investigation into SCLC pathogenesis and potential therapeutic strategies.

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