Alternative splicing of the p53 tumor suppressor gene in the Molt-4 T-lymphoblastic leukemia cell line

Chow, Vincent T.K.; Quek, H.H.; Tock, Edward P.C.

doi:10.1016/0304-3835(93)90256-9

Cited by 59RNA Research and SplicingCancer-related Molecular PathwaysCancer-related molecular mechanisms research

Alternative splicing of the p53 tumor suppressor gene in the Molt-4 T-lymphoblastic leukemia cell line

Chow, Vincent T.K., Quek, H.H., Tock, Edward P.C.·1993·Cancer Letters

DOI 10.1016/0304-3835(93)90256-9

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Abstract

The expression of the p53 tumor suppressor gene in ten human cell lines (nine cancers and one normal) was studied using reverse transcription, polymerase chain reaction (PCR) and direct sequencing. Using P53U and P53D primers for amplifying a 371-base pair (bp) target fragment spanning exons 7-10 of p53 cDNA, normal-sized PCR products were amplified from 9 cell lines but not from the Hep3B hepatocellular carcinoma (HCC) cell line. An additional larger band (504 bp) was observed for the Molt-4 T-lymphoblastic leukemia cell line. Employing P531 and P53D primers which flank a 76-bp p53 cDNA fragment, 76 bp as well as 209 bp products were generated by PCR of Molt-4 cDNA. Direct sequencing of the 504 bp and 209 bp bands confirmed the presence of a 133 bp insertion between exons 9 and 10 in the aberrant transcript. This insertion was homologous to a 130-bp sequence within the wild-type p53 intron 9, except for 2 point mutations and 3 base insertions. Sequencing of P53U/P53D PCR products of Molt-4 genomic DNA revealed an 8 bp deletion just downstream to the 133 bp insertion, creating a novel donor splicing site within intron 9. This site, coupled with an inherent acceptor splicing site just upstream to the 133 bp insertion, suggests that the 133 bp stretch represents an alternative exon. The occurrence of a termination signal within this alternative transcript is predicted to culminate in a truncated p53 translational product. The sequences of the 371 bp PCR products of Molt-4, HT-1…

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The RAJI cell line harbors the loss-of-function mutant alleles R213Q and Y234H.
“The cell line RAJI, which harbors the loss-of-function mutant alleles R213Q and Y234H [34–36] for p53 targets including TLR3 and p21 (Supplementary Figure S4A), was treated with the reactivating drugs RITA [36] and PRIMA-1 [37] as well as with the anticancer drugs doxorubicin (DXR) and 5-fluorouracil (5FU) to induce p53.”
From Ligand dependent restoration of human TLR3 signaling and death in p53 mutant cells (2016) · cites this paper as [34]

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Authors: Chow, V. T. K., Quek, H. H., & Tock, E. P. C.
Affiliations: National University of Singapore (SG)
Corresponding author: Chow, Vincent T.K.
ORCID: Chow, Vincent T.K.
Venue: Cancer Letters
Publisher: Elsevier BV
Published: 1993-09
Volume: 73
Issue: 2-3
Pages: 141-148
ISSN: 0304-3835 (ISSN-L)
DOI: 10.1016/0304-3835(93)90256-9
OpenAlex: W2000937841
Cited by: 59
References: 46
Citations by year: 2023: 2 · 2022: 1 · 2017: 1 · 2016: 2 · 2014: 1 · 2012: 2
FWCI: 0.90
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Cancer Letters (publishedVersion)
PubMed (publishedVersion)
National University of Singapore (submittedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
Keywords: p53, alternative splicing, MOLT-4 cells, T-cell acute lymphoblastic leukemia, alternative exons, TP53 mutation, hepatocellular carcinoma, Burkitt lymphoma, tumor suppressor gene expression
MeSH terms: Amino Acid Sequence, Base Sequence, DNA, Neoplasm, Humans, Molecular Sequence Data, Transcription, Genetic, Tumor Cells, Cultured, Leukemia-Lymphoma, Adult T-Cell, Gene Expression, Polymerase Chain Reaction, Genes, p53, Alternative Splicing, Sequence Analysis, DNA

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Alternative splicing of the p53 tumor suppressor gene in the Molt-4 T-lymphoblastic leukemia cell line

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