ArticlePloS one2012
Tumour suppressive function and modulation of programmed cell death 4 (PDCD4) in ovarian cancer.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 60 citations in OpenAlex.
- Functional characterisation of tumour suppressor PDCD4 reveals previously undisclosed role in the control of cell adhesion.Nucleic acids research · 2026Article
- Covalent Inhibition of the Peptidyl-Prolyl Isomerase Pin1 by Sulfopin Results in a Broad Impact on the Phosphoproteome of Human Osteosarcoma U2-OS Cells.Proteomics · 2025Article
- MicroRNA-21 Promotes the Viability, Proliferation and Milk Fat Synthesis of Ovine Mammary Epithelial Cells by TargetingInternational journal of molecular sciences · 2025Article
- Exosomal insights into ovarian cancer stem cells: revealing the molecular hubs.Journal of ovarian research · 2025Article
- Non-coding RNA transcripts, incredible modulators of cisplatin chemo-resistance in bladder cancer through operating a broad spectrum of cellular processes and signaling mechanism.Non-coding RNA research · 2024Review
- Neuronal activity regulates the nuclear proteome to promote activity-dependent transcription.The Journal of cell biology · 2021Article
- Combined Inhibition of AKT and KIT Restores Expression of Programmed Cell Death 4 (PDCD4) in Gastrointestinal Stromal Tumor.Cancers · 2021Article
- SNPs in miRNAs and Target Sequences: Role in Cancer and Diabetes.Frontiers in genetics · 2021Review
- Article
- PDCD4 controls the G1/S-phase transition in a telomerase-immortalized epithelial cell line and affects the expression level and translation of multiple mRNAs.Scientific reports · 2020Article
- Multiple Myeloma Cells Alter Adipogenesis, Increase Senescence-Related and Inflammatory Gene Transcript Expression, and Alter Metabolism in Preadipocytes.Frontiers in oncology · 2020Article
- Roles of microRNAs in Ovarian Cancer Tumorigenesis: Two Decades Later, What Have We Learned?Frontiers in oncology · 2020Review
- EIF3H interacts with PDCD4 enhancing lung adenocarcinoma cell metastasis.American journal of cancer research · 2020Article
- Combined inhibition of the PI3K/mTOR/MEK pathway induces Bim/Mcl-1-regulated apoptosis in pancreatic cancer cells.Cancer biology & therapy · 2019Article
- MiR-1260b inhibitor enhances the chemosensitivity of colorectal cancer cells to fluorouracil by targeting PDCD4/IGF1.Oncology letters · 2018Article
- The role of Pdcd4 in tumour suppression and protein translation.Biology of the cell · 2018Review
- Retracted Article: Linc00472 suppresses breast cancer progression and enhances doxorubicin sensitivity through regulation of miR-141 and programmed cell death 4.RSC advances · 2018Article
- Inhibition of cell migration and invasion and promotion of cell apoptosis by overexpression of programmed cell death 4 (PDCD4) in cervical cancer Siha cells.International journal of clinical and experimental pathology · 2018Article
- Tumor suppressor Pdcd4 attenuates Sin1 translation to inhibit invasion in colon carcinoma.Oncogene · 2017Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundProgrammed cell death 4 (PDCD4), originally identified as the neoplastic transformation inhibitor, was attenuated in various cancer types. Our previous study demonstrated a continuous down-regulation of PDCD4 expression in the sequence of normal-borderline-malignant ovarian tissue samples and a significant correlation of PDCD4 expression with disease-free survival. The objective of the current study was to further investigate the function and modulation of PDCD4 in ovarian cancer cells. PRINCIPAL
findingsWe demonstrated that ectopic PDCD4 expression significantly inhibited cell proliferation by inducing cell cycle arrest at G(1) stage and up-regulation of cell cycle inhibitors of p27 and p21. Cell migration and invasion were also inhibited by PDCD4. PDCD4 over-expressing cells exhibited elevated phosphatase and tensin homolog (PTEN) and inhibited protein kinase B (p-Akt). In addition, the expression of PDCD4 was up-regulated and it was exported to the cytoplasm upon serum withdrawal treatment, but it was rapidly depleted via proteasomal degradation upon serum re-administration. Treatment of a phosphoinositide 3-kinase (PI3K) inhibitor prevented the degradation of PDCD4, indicating the involvement of PI3K-Akt pathway in the modulation of PDCD4.
conclusionPDCD4 may play a critical function in arresting cell cycle progression at key checkpoint, thus inhibiting cell proliferation, as well as suppressing tumour metastasis. The PI3K-Akt pathway was implied to be involved in the regulation of PDCD4 degradation in ovarian cancer cells. In response to the stress condition, endogenous PDCD4 was able to shuttle between cell compartments to perform its diverted functions.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.