Characterization of programmed cell death 4 in multiple human cancers reveals a novel enhancer of drug sensitivity

Jansen, Aaron P.; Camalier, Corinne E.; Stark, Cristi; Colburn, Nancy H.

doi:10.1158/1535-7163.103.3.2

Cited by 133Cancer-related Molecular PathwaysCell death mechanisms and regulationPI3K/AKT/mTOR signaling in cancer

Characterization of programmed cell death 4 in multiple human cancers reveals a novel enhancer of drug sensitivity

Jansen, Aaron P., Camalier, Corinne E., Stark, Cristi, Colburn, Nancy H.·2004·Molecular Cancer Therapeutics

DOI 10.1158/1535-7163.103.3.2

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Abstract

Programmed cell death 4 (Pdcd4), originally identified as an inhibitor of murine cellular transformation, inhibits protein synthesis by directly interacting with eukaryotic initiation factor 4A (eIF4A) of the translation initiation complex. The relevance of Pdcd4 to a broad range of human cancers derived from multiple tissue sites is unknown. Protein expression patterns from the National Cancer Institute drug-screening panel of 60 human cancer cells (NCI60) were analyzed by Western blot methods and revealed frequent reduction of Pdcd4 protein levels in renal-, lung-, and glia-derived tumors. Greater than mean Pdcd4 protein levels correlated with the antitumor activity of geldanamycin and tamoxifen. Stable expression of antisense PDCD4 significantly reduced the sensitivity of MCF-7 breast cancer cells to geldanamycin and to tamoxifen. Sensitivity to geldanamycin significantly increased in UO-31 renal cancer cells expressing sense PDCD4 cDNA. Increased geldanamycin sensitivity was accompanied by enhanced cell cycle arrest and apoptosis. One primary mode of inactivation of Pdcd4 in human cancers appears to involve down-regulated expression, and this down-regulation causes a decreased sensitivity to geldanamycin cytotoxicity. Thus, up-regulating Pdcd4 expression may be promising for geldanamycin-based combination therapy.

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PDCD4 upregulation sensitizes tumor cells to anti-tumor drugs such as cisplatin, gemcitabine, geldanamycin, and tamoxifen.
“It has been reported that PDCD4 upregulation sensitizes tumor cells to anti-tumor drugs such as cisplatin [104], gemcitabine [102], geldanamycin and tamoxifen [105].”
From Control Mechanisms of the Tumor Suppressor PDCD4: Expression and Functions (2019) · cites this paper as [105]

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がん抑制遺伝子Programmed cell death 4(Pdcd4)の発現量とがん細胞浸潤能の関係
中村一基, & 吉川紀子 (2015)

Authors: Jansen, A. P., Camalier, C. E., Stark, C., & Colburn, N. H.
Affiliations: Frederick National Laboratory for Cancer Research (US)
Venue: Molecular Cancer Therapeutics
Publisher: American Association for Cancer Research (AACR)
Published: 2004-02-01
Volume: 3
Issue: 2
Pages: 103-110
ISSN: 1535-7163 (ISSN-L)
1538-8514
DOI: 10.1158/1535-7163.103.3.2
OpenAlex: W2257484201
Cited by: 132
References: 46
Citations by year: 2025: 2 · 2024: 2 · 2023: 3 · 2022: 6 · 2021: 4 · 2020: 4 · 2019: 4 · 2018: 2 · 2017: 4 · 2016: 4 · 2015: 6 · 2014: 9 · 2013: 6 · 2012: 9
FWCI: 3.36
Type: journal article
Language: en
Open access: closed
Locations: Molecular Cancer Therapeutics (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Keywords: PDCD4, eIF4A, translation initiation, drug sensitivity, geldanamycin, tamoxifen, kidney cancer, breast cancer, apoptosis, cell cycle arrest, combination therapy, tumor suppressor
MeSH terms: Antineoplastic Agents, Cell Division, Drug Screening Assays, Antitumor, Humans, Kidney Neoplasms, Mitosis, Neoplasms, Prognosis, Quinones, RNA, Messenger, Tamoxifen, Retinoblastoma Protein, G2 Phase, Benzoquinones, Tacrolimus, RNA-Binding Proteins, Cell Line, Tumor, Lactams, Macrocyclic, Apoptosis Regulatory Proteins

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Characterization of programmed cell death 4 in multiple human cancers reveals a novel enhancer of drug sensitivity

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