Programmed Cell Death 4 (PDCD4) Is an Important Functional Target of the MicroRNA miR-21 in Breast Cancer Cells*
By Lisa B. Frankel, N. R. Christoffersen, Anders Jacobsen, M. Lindow, Anders Krogh, A. Lund. Journal of Biological Chemistry, 2008
1,123 citations recorded by the source corpus.
MicroRNAs are emerging as important regulators of cancer-related processes. The miR-21 microRNA is overexpressed in a wide variety of cancers and has been causally linked to cellular proliferation, apoptosis, and migration. Inhibition of mir-21 in MCF-7 breast cancer cells causes reduced cell growth. Using array expression analysis of MCF-7 cells depleted of miR-21, we have identified mRNA targets of mir-21 and have shown a link between miR-21 and the p53 tumor suppressor protein. We furthermore found that the tumor suppressor protein Programmed Cell Death 4 (PDCD4) is regulated by miR-21 and demonstrated that PDCD4 is a functionally important target for miR-21 in breast cancer cells.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/2ea313a808599cb2e910720411e897cd6097ba5e
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In Cancer Research
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Citations in the corpus
- MicroRNA and cancer (2012, background): “Mechanistically, this has been explained through the identification of key downstream target genes, such as PTEN, PDCD4 and SPRY1 (Frankel et al., 2008; Meng et al., 2007; Thum et al., 2008).”
- Non-coding RNAs as regulators of embryogenesis (2011, background): “It represses tumour suppressors such as programmed cell death 4 ( PDCD4 ) and phosphatase and tensin homologue ( PTEN”
- miR-21: a small multi-faceted RNA (2008, background): “It is also worth noting that miR-21 inhibition leads to the reduced expression of several critical oncogenes, including MYC, Jun, RELB and LIF, and MYC reduction was also detected by a similar analysis performed on breast cancer MCF7 cells [53].”
- Silencing of microRNA families by seed-targeting tiny LNAs (2011, background): “This coincided with sequestration of miR-21 in a slower-migrating heteroduplex with antimiR-21, de-repression of HeLa mRNAs with canonical miR-21 seed match sites and upregulation of the Pdcd4 target protei”
- MicroRNA-21 targets a network of key tumor-suppressive pathways in glioblastoma cells. (2008, background): “A subset of the derepressed transcripts, APAF1, BMPR2, PDCD4, and p21 were reported to be up-regulated in MCF-7 breast cancer cells with LNA-miR-21 treatment (15).”
- MicroRNA-10a binds the 5'UTR of ribosomal protein mRNAs and enhances their translation. (2008, background): “, 2005) or endogenous miRNAs have been inhibited following transfections with miRNA-inhibitory oligonucleotides (Frankel et al., 2007; Krutzfeldt et al., 2005).”
- MicroRNA 21 Promotes Glioma Invasion by Targeting Matrix Metalloproteinase Regulators (2008, background): “material) have recently been identified in an mRNA expression analysis of miR-21 knocked-down MCF7 breast carcinoma cells (14).”
- Negative regulation of TLR4 via targeting of the proinflammatory tumor suppressor PDCD4 by the microRNA miR-21 (2010, background): “The miRNA miR-21 targets Pdcd4 mRNA post-transcriptionally, blocking production of PDCD4 protei”
- MicroRNA dysregulation in cancer: diagnostics, monitoring and therapeutics. A comprehensive review (2012, neutral): “Additional studies showed that miR-21 anti-apoptotic effects occurs by targeting the tumour suppressors phosphatase and tensin homologue (PTEN) and programmed cell death 4 (PDCD4) (Frankel et al, 2008; Meng et al, 2007).”
- MicroRNA function in cancer: oncogene or a tumor suppressor? (2009, background): “miR-21 also down-regulates tumor suppressor geneprogrammed cell death-4, which, at least in part, contributes to the effects of miR-21 on cellular proliferation [67].”
- Modulation of K-ras-dependent lung tumorigenesis by microRNA-21 (2010, positive): “PDCD4 is a proapoptotic tumor suppressor gene and has been verified as a miR-21 target in human colorectal and breast cancer cell lines (Afonja et al., 2004; Asangani et al., 2008; Bitomsky et al., 2008; Frankel et al., 2008; Lu et al., 2008; Zhang et al., 2006).”