ArticleOncotarget2013
Small molecule-induced mitochondrial disruption directs prostate cancer inhibition via UPR signaling.
Article in Oncotarget, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 33 citations in OpenAlex.
- Upregulated SKP2 Empowers Epidermal Proliferation Through Downregulation of P27 Kip1.Annals of dermatology · 2024Article
- Small-molecule compounds inhibiting S-phase kinase-associated protein 2: A review.Frontiers in pharmacology · 2023Review
- The Intertwined Roles of Oxidative Stress and Endoplasmic Reticulum Stress in Glaucoma.Antioxidants (Basel, Switzerland) · 2022Review
- Dual roles of HSP70 chaperone HSPA1 in quality control of nascent and newly synthesized proteins.The EMBO journal · 2021Article
- [Targeting Cullin-RING E3 ligases for anti-cancer therapy: efforts on drug discovery].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020Review
- The Role of the ER-Induced UPR Pathway and the Efficacy of Its Inhibitors and Inducers in the Inhibition of Tumor Progression.Oxidative medicine and cellular longevity · 2019Review
- Mitochondrial biology and prostate cancer ethnic disparity.Carcinogenesis · 2018Review
- A patent review of the ubiquitin ligase system: 2015-2018.Expert opinion on therapeutic patents · 2018Review
- Oxidized analogs of Di(1Oncotarget · 2018Article
- A mitochondria-targeted nanoradiosensitizer activating reactive oxygen species burst for enhanced radiation therapy.Chemical science · 2018Article
- Tannic Acid Induces Endoplasmic Reticulum Stress-Mediated Apoptosis in Prostate Cancer.Cancers · 2018Article
- Metabolic coupling and the Reverse Warburg Effect in cancer: Implications for novel biomarker and anticancer agent development.Seminars in oncology · 2017Review
- Mitochondria, cholesterol and cancer cell metabolism.Clinical and translational medicine · 2016Review
- Article
- Anticancer drugs for the modulation of endoplasmic reticulum stress and oxidative stress.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Review
- Article
- WWOX suppresses prostate cancer cell progression through cyclin D1-mediated cell cycle arrest in the G1 phase.Cell cycle (Georgetown, Tex.) · 2015Article
- Cancer Microenvironment and Endoplasmic Reticulum Stress Response.Mediators of inflammation · 2015Review
- Is reliance on mitochondrial respiration a "chink in the armor" of therapy-resistant cancer?Cancer cell · 2014Article
- SKP2 E3 ligase in urological malignancies: a critical regulator of the cell cycle and therapeutic target.Cell cycle (Georgetown, Tex.)Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
We previously identified SMIP004 (N-(4-butyl-2-methyl-phenyl) acetamide) as a novel inducer of cancer-cell selective apoptosis of human prostate cancer cells. SMIP004 decreased the levels of positive cell cycle regulators, upregulated cyclin-dependent kinase inhibitors, and resulted in G1 arrest, inhibition of colony formation in soft agar, and cell death. However, the mechanism of SMIP004-induced cancer cell selective apoptosis remained unknown. Here, we used chemical genomic and proteomic profiling to unravel a SMIP004-induced pro-apoptotic pathway, which initiates with disruption of mitochondrial respiration leading to oxidative stress. This, in turn, activates two pathways, one eliciting cell cycle arrest by rapidly targeting cyclin D1 for proteasomal degradation and driving the transcriptional downregulation of the androgen receptor, and a second pathway that activates pro-apoptotic signaling through MAPK activation downstream of the unfolded protein response (UPR). SMIP004 potently inhibits the growth of prostate and breast cancer xenografts in mice. Our data suggest that SMIP004, by inducing mitochondrial ROS formation, targets specific sensitivities of prostate cancer cells to redox and bioenergetic imbalances that can be exploited in cancer therapy.
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.