Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis

Chang, Tsung-Cheng; Wentzel, Erik A.; Kent, Oliver A.; Ramachandran, Kalyani; Mullendore, Michael; Lee, Kwang Hyuck; Feldmann, Georg; Yamakuchi, Munekazu; Ferlito, Marcella; Lowenstein, Charles J.; Arking, Dan E.; Beer, Michael A.; Maitra, Anirban; Mendell, Joshua T.

doi:10.1016/j.molcel.2007.05.010

Cited by 2,010MicroRNA in disease regulationCancer-related Molecular PathwaysCancer-related molecular mechanisms research

Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis

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Chang, Tsung-Cheng, Wentzel, Erik A., Kent, Oliver A., Ramachandran, Kalyani, Mullendore, Michael, Lee, Kwang Hyuck, Feldmann, Georg, Yamakuchi, Munekazu +6 more·2007·Molecular Cell

DOI 10.1016/j.molcel.2007.05.010PMC PMC1939978

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Abstract

The p53 tumor suppressor protein is a critical regulator of the cellular response to cancer-initiating insults such as genotoxic stress. In this report, we demonstrate that microRNAs (miRNAs) are important components of the p53 transcriptional network. Global miRNA expression analyses identified a cohort of miRNAs that exhibit p53-dependent upregulation following DNA damage. One such miRNA, miR-34a, is commonly deleted in human cancers and, as shown here, frequently absent in pancreatic cancer cells. Characterization of the miR-34a primary transcript and promoter demonstrates that this miRNA is directly transactivated by p53. Expression of miR-34a causes dramatic reprogramming of gene expression and promotes apoptosis. Much like the known set of p53-regulated genes, miR-34a-responsive genes are highly enriched for those that regulate cell-cycle progression, apoptosis, DNA repair, and angiogenesis. Therefore, it is likely that an important function of miR-34a is the modulation and fine-tuning of the gene expression program initiated by p53.

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The genetic interaction network landscape had edges consistently supported by changes found in a microarray study identifying transcripts altered downstream of miR34-a.
“Considering other proteins significantly changed in AsymAD, like TMPO and HNRNPF (Table S2), the genetic interaction network landscape had edges that were consistently supported by changes found in a microarray study which identified transcripts altered downstream of an age-associated overexpressed circulating and brain-resident microRNA, mIR34-a (Chang et al., 2007; Li et al., 2011).”
From A Multi-network Approach Identifies Protein-Specific Co-expression in Asymptomatic and Symptomatic Alzheimer’s Disease (2017) · cites this paper as Chang et al., 2007

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Authors: Chang, T.-C., Wentzel, E. A., Kent, O. A., Ramachandran, K., Mullendore, M., Lee, K. H., Feldmann, G., Yamakuchi, M., Ferlito, M., Lowenstein, C. J., Arking, D. E., Beer, M. A., Maitra, A., & Mendell, J. T.
Affiliations: Johns Hopkins University (US)
Corresponding author: Mendell, Joshua T.
ORCID: Chang, Tsung-Cheng
Kent, Oliver A.
Ramachandran, Kalyani
Lee, Kwang Hyuck
Feldmann, Georg
Yamakuchi, Munekazu
Lowenstein, Charles J.
Arking, Dan E.
Beer, Michael A.
Maitra, Anirban
Mendell, Joshua T.
Venue: Molecular Cell
Publisher: Elsevier BV
Published: 2007-06
Volume: 26
Issue: 5
Pages: 745-752
ISSN: 1097-2765 (ISSN-L)
DOI: 10.1016/j.molcel.2007.05.010
PMC: PMC1939978
OpenAlex: W2038167014
Cited by: 2,010
References: 59
Citations by year: 2026: 23 · 2025: 37 · 2024: 34 · 2023: 47 · 2022: 54 · 2021: 94 · 2020: 84 · 2019: 89 · 2018: 94 · 2017: 116 · 2016: 121 · 2015: 133 · 2014: 186 · 2013: 159 · 2012: 177
FWCI: 45.22
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 2274 d)
Locations: Molecular Cell (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: Rita Allen Foundation
Lustgarten Foundation
Allen Foundation
National Cancer Institute (R01CA113669, R01CA120185)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
Keywords: miR-34a, p53, DNA damage response, apoptosis, gene expression reprogramming, pancreatic cancer, cell cycle regulation, DNA repair, angiogenesis, tumor suppressor
MeSH terms: Base Sequence, DNA Damage, Humans, Pancreatic Neoplasms, Promoter Regions, Genetic, RNA, Neoplasm, Transcriptional Activation, Gene Expression, Tumor Suppressor Protein p53, Apoptosis, MicroRNAs, Cell Line, Tumor

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Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis

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