ReviewSeminars in cancer biology2021
Connections between endoplasmic reticulum stress-associated unfolded protein response, mitochondria, and autophagy in arsenic-induced carcinogenesis.
Review in Seminars in cancer biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 119 citations in OpenAlex.
- Multifunctional nanotherapeutics for targeted modulation of endoplasmic reticulum stress to potentiate cancer therapy.Asian journal of pharmaceutical sciences · 2026Review
- Understanding the contribution of toxicant exposures to Alzheimer's disease and related dementias.Current opinion in neurobiology · 2026Review
- A TFAP4-UBC9-SUMO1 axis orchestrates pathological mitochondrial hyperfission in diabetic complications.Acta diabetologica · 2026Article
- The gut-brain axis in arsenic-induced toxicity: mechanisms, consequences, and therapeutic perspectives.Metabolic brain disease · 2026Review
- Novel Phosphatase SSU72 Drives Malignant Progression in Colorectal Cancer via PERKInternational journal of biological sciences · 2026Article
- Expression and role of HSPA5 in environmental toxin-induced neurological disorders.Frontiers in molecular neuroscience · 2026Review
- Prime editing links the split integrated stress response to pathogenic eIF2B mutations and white matter degeneration.Cell death & disease · 2025Article
- Arsenic Trioxide Underpins Delayed Neuroinflammation and Impaired Synaptic Integrity involving Integrative Stress Response Signaling.bioRxiv : the preprint server for biology · 2025Article
- Chronic arsenic exposure and hsa-miR-186 overexpression causes transcriptome-wide differential alternative splicing contributing to skin carcinogenesis in human HaCaT cell line.Archives of toxicology · 2025Article
- Arsenic-induced nephrotoxicity: Mechanisms, biomarkers, and preventive strategies for global health.Veterinary world · 2025Review
- TRAF3IP3 Induces ER Stress-Mediated Apoptosis with Protective Autophagy to Inhibit Lung Adenocarcinoma Proliferation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Sigma-1 Receptor Specific Biological Functions, Protective Role, and Therapeutic Potential in Cardiovascular Diseases.Cardiovascular toxicology · 2025Review
- An integrated machine learning framework for developing and validating a prognostic risk model of gastric cancer based on endoplasmic reticulum stress-associated genes.Biochemistry and biophysics reports · 2025Article
- Inorganic arsenic modulates cell apoptosis by regulating Argonaute 2 expression via the p53 pathway.Toxicology research · 2025Article
- Cyclometalated iridium(III) complex based on isoquinoline alkaloid synergistically elicits the ICD response and IDO inhibitionActa pharmaceutica Sinica. B · 2025Article
- Article
- Article
- Multiple roles of arsenic compounds in phase separation and membraneless organelles formation determine their therapeutic efficacy in tumors.Journal of pharmaceutical analysis · 2024Review
- Norcantharidin inhibits the malignant progression of cervical cancer by inducing endoplasmic reticulum stress.Molecular medicine reports · 2024Article
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 at 2 institutions in 1 country.
Funding
Abstract
Arsenic exposure in contaminated drinking water is a global health issue, as more than 200 million people are affected globally. Arsenic has been known to cause skin, liver, lung, bladder and prostate cancers. Accordingly, it has been categorized as a group I human carcinogen by the International Agency for Research on Cancer (IARC). Various natural and anthropogenic activities lead to the release of arsenic in the environment, contaminating air, water and food sources. Traditionally, genetic mutations have been the center of cancer research. However, emerging studies have now focused on the importance of epigenetics, metabolism and endoplasmic reticulum (ER) stress in cancer. Arsenic is highly capable of inducing stress in the cells via the generation of free radicals causing oxidative stress, epigenetic and genetic alterations, mitochondrial dysfunction, activation of intracellular signaling pathways, and impairment of autophagy and DNA repair systems. The cancer cells are able to utilize the unfolded protein response (UPR) to overcome these internal stresses in various stages of arsenic-induced carcinogenesis, from cancer growth to immune responses. The UPR is an evolutionarily conserved stress response that has both survival and apoptotic outcomes. PERK, IRE1α and ATF6α are the three ER stress sensors that are activated to maintain cellular proteostasis, which can also promote apoptosis on prolonged ER stress. The dual nature of UPR in different cancer types and stages is a challenge for researchers. We must investigate the role and the connections among ER stress-associated UPR, mitochondrial dysfunction and autophagy in arsenic malignancies to identify key targets for cancer prevention and therapeutics.
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.