ReviewInternational journal of molecular sciences2020
A New Twist in Protein Kinase B/Akt Signaling: Role of Altered Cancer Cell Metabolism in Akt-Mediated Therapy Resistance.
Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 33 citations in OpenAlex.
- Combinatorial Treatment with Chlorogenic Acid and Cinnamaldehyde Disrupts Intracellular pH and Metabolic Transport in Breast Cancer Cells.Molecules (Basel, Switzerland) · 2026Article
- Role of epithelial-mesenchymal transition (EMT) in malignancies: current status and future prospects.Signal transduction and targeted therapy · 2026Review
- Sangyod rice extract attenuates oleic acid-induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways.Food chemistry. Molecular sciences · 2026Article
- A mitochondrial regulatory network of ferroptosis defense in HPV-positive cervical cancer: therapeutic implications of the mitoSTAT3-DHODH axis.Frontiers in pharmacology · 2026Review
- Chromium as a Modulator of Insulin Receptor Activity: A Systematic Review of Its Role in Metabolic Syndrome and Type 2 Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Diversity of oxidative stress and senescence phenotypes induced by chemotherapeutic agents in HUVECs.Scientific reports · 2025Article
- Oxidative Stress and Redox Imbalance: Common Mechanisms in Cancer Stem Cells and Neurodegenerative Diseases.Cells · 2025Review
- Application of Nanotechnology and Phytochemicals in Anticancer Therapy.Pharmaceutics · 2024Review
- Modulating DNA damage response in uveal melanoma through embryonic stem cell microenvironment.BMC cancer · 2024Article
- SDC4-rs1981429 and ATM-rs228590 may provide early biomarkers of breast cancer risk.Journal of cancer research and clinical oncology · 2023Article
- Nur77 Serves as a Potential Prognostic Biomarker That Correlates with Immune Infiltration and May Act as a Good Target for Prostate adenocarcinoma.Molecules (Basel, Switzerland) · 2023Article
- HDAC-an important target for improving tumor radiotherapy resistance.Frontiers in oncology · 2023Review
- Impacts of Oxidative Stress and PI3K/AKT/mTOR on Metabolism and the Future Direction of Investigating Fucoidan-Modulated Metabolism.Antioxidants (Basel, Switzerland) · 2022Review
- ROS-Mediated Enamel Formation Disturbance Characterized by Alternative Cervical Loop Cell Proliferation and Downregulation of RhoA/ROCK in Ameloblasts.Oxidative medicine and cellular longevity · 2022Article
- High glucose-induced inhibition of osteoblast like MC3T3-E1 differentiation promotes mitochondrial perturbations.PloS one · 2022Article
- Targeting AKT-Dependent Regulation of Antioxidant Defense Sensitizes AKT-E17K Expressing Cancer Cells to Ionizing Radiation.Frontiers in oncology · 2022Article
- Metabolism of cancer cells commonly responds to irradiation by a transient early mitochondrial shutdown.iScience · 2021Article
- Article
- Rapamycin Plus Doxycycline Combination Affects Growth Arrest and Selective Autophagy-Dependent Cell Death in Breast Cancer Cells.International journal of molecular sciences · 2021Article
- DNA damage repair: historical perspectives, mechanistic pathways and clinical translation for targeted cancer therapy.Signal transduction and targeted therapy · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cancer resistance to chemotherapy, radiotherapy and molecular-targeted agents is a major obstacle to successful cancer therapy. Herein, aberrant activation of the phosphatidyl-inositol-3-kinase (PI3K)/protein kinase B (Akt) pathway is one of the most frequently deregulated pathways in cancer cells and has been associated with multiple aspects of therapy resistance. These include, for example, survival under stress conditions, apoptosis resistance, activation of the cellular response to DNA damage and repair of radiation-induced or chemotherapy-induced DNA damage, particularly DNA double strand breaks (DSB). One further important, yet not much investigated aspect of Akt-dependent signaling is the regulation of cell metabolism. In fact, many Akt target proteins are part of or involved in the regulation of metabolic pathways. Furthermore, recent studies revealed the importance of certain metabolites for protection against therapy-induced cell stress and the repair of therapy-induced DNA damage. Thus far, the likely interaction between deregulated activation of Akt, altered cancer metabolism and therapy resistance is not yet well understood. The present review describes the documented interactions between Akt, its target proteins and cancer cell metabolism, focusing on antioxidant defense and DSB repair. Furthermore, the review highlights potential connections between deregulated Akt, cancer cell metabolism and therapy resistance of cancer cells through altered DSB repair and discusses potential resulting therapeutic implications.
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.