ReviewExperimental oncology2012
Caspase control: protagonists of cancer cell apoptosis.
Review in Experimental oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 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
124 citing papers in PubMed.
- A Randomised, Double Blind, Placebo-Controlled Pilot Study of Oral Artesunate Therapy for Colorectal Cancer.EBioMedicine · 2015Trial
- DNA methylation-mediated regulation of TRAIL pathway components (DR5, DcR2, and CASP3) in breast cancer: molecular mechanisms and therapeutic implications.Molecular biology reports · 2026Review
- Carotenoid-Rich Pigment Extract From Micrococcus terreus SK34 Induces Apoptosis in SH-SY5Y Neuroblastoma Cells: Integrated Metabolomic, Molecular Docking, and Experimental Validation.MicrobiologyOpen · 2026Article
- Article
- Discovery of potent bisindole-based pyrazolopyridine derivatives as topoisomerase inhibitors: DNA damage induction and synergistic antileukemic activity.Frontiers in pharmacology · 2026Article
- The interconnection between androgen receptor and DNA damage response pathways in prostate cancer.Current urology · 2025Review
- Activation of Hippocampal ACE2 Prevents the Dysbiosis-induced Depression-like Behavior in Mice by Enhanced Neurogenesis and Neuroprotection via Mas Receptor.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Medical Potential of Insect Symbionts.Insects · 2025Review
- Polygenic anti-cancer activity ofToxicology reports · 2024Article
- A self-immolative near-infrared fluorescent probe for identification of cancer cells and facilitating its apoptosis.Analytical and bioanalytical chemistry · 2024Article
- Optogenetic induction of caspase-8 mediated apoptosis by employing Arabidopsis cryptochrome 2.Scientific reports · 2023Article
- Article
- Visualization of breast cancer-related protein synthesis from the perspective of bibliometric analysis.European journal of medical research · 2023Article
- Inhibitory effect of O-propargyllawsone in A549 lung adenocarcinoma cells.BMC complementary medicine and therapies · 2023Article
- Potential Chemopreventive Role of Pterostilbene in Its Modulation of the Apoptosis Pathway.International journal of molecular sciences · 2023Review
- The Anti-Proliferative and Apoptotic Effects of Rutaecarpine on Human Esophageal Squamous Cell Carcinoma Cell Line CE81T/VGH In Vitro and In Vivo.International journal of molecular sciences · 2022Article
- Identification of 20(Oxidative medicine and cellular longevity · 2022Article
- Role of the JNK Pathway in Bladder Cancer.OncoTargets and therapy · 2022Review
- The m6A-induced lncRNA CASC8 promotes proliferation and chemoresistance via upregulation of hnRNPL in esophageal squamous cell carcinoma.International journal of biological sciences · 2022Article
- Gadolinium chloride pre-treatment reduces the inflammatory response and preserves intestinal barrier function in a rat model of sepsis.Experimental and therapeutic medicine · 2021Article
64 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Emergence of castration-resistant metastatic prostate cancer is due to activation of survival pathways, including apoptosis suppression and anoikis resistance, and increased neovascularization. Thus targeting of apoptotic players is of critical significance in prostate cancer therapy since loss of apoptosis and resistance to anoikis are critical in aberrant malignant growth, metastasis and conferring therapeutic failure. The majority of therapeutic agents act through intrinsic mitochondrial, extrinsic death receptor pathways or endoplasmic reticulum stress pathways to induce apoptosis. Current therapeutic strategies target restoring regulatory molecules that govern the pro-survival pathways such as PTEN which regulates AKT activity. Other strategies focus on reactivating the apoptotic pathways either by down-regulating anti-apoptotic players such as BCL-2 or by up-regulating pro-apoptotic protein families, most notably, the caspases. Caspases are a family of cystine proteases which serve critical roles in apoptotic and inflammatory signaling pathways. During tumorigenesis, significant loss or inactivation of lead members in the caspase family leads to impairing apoptosis induction, causing a dramatic imbalance in the growth dynamics, ultimately resulting in aberrant growth of human cancers. Recent exploitation of apoptosis pathways towards re-instating apoptosis induction via caspase re-activation has provided new molecular platforms for the development of therapeutic strategies effective against advanced prostate cancer as well as other solid tumors. This review will discuss the current cellular landscape featuring the caspase family in tumor cells and their activation via pharmacologic intervention towards optimized anti-cancer therapeutic modalities. This article is part of a Special Issue entitled "Apoptosis: Four Decades Later".
Indexed as
Identifiers
23070001PMC3721730What 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.