ReviewCell cycle (Georgetown, Tex.)2018
The macroenviromental control of cancer metabolism by p62.
Review in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 17 citations in OpenAlex.
- The Roles of SQSTM1/p62 in Selective Autophagy and Oncogenic Signaling.International journal of molecular sciences · 2026Review
- From Crypts to Cancer: A Holistic Perspective on Colorectal Carcinogenesis and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Cancer-Associated Adipocytes and Breast Cancer: Intertwining in the Tumor Microenvironment and Challenges for Cancer Therapy.Cancers · 2023Review
- p62 functions as a signal hub in metal carcinogenesis.Seminars in cancer biology · 2021Review
- CUL5-ASB6 Complex Promotes p62/SQSTM1 Ubiquitination and Degradation to Regulate Cell Proliferation and Autophagy.Frontiers in cell and developmental biology · 2021Article
- Chronic Isolation Stress Affects Central Neuroendocrine Signaling Leading to a Metabolically Active Microenvironment in a Mouse Model of Breast Cancer.Frontiers in behavioral neuroscience · 2021Article
- p62: Friend or Foe? Evidences forInternational journal of molecular sciences · 2020Review
- Overexpression of Hepatocyte Chemerin-156 Lowers Tumor Burden in a Murine Model of Diethylnitrosamine-Induced Hepatocellular Carcinoma.International journal of molecular sciences · 2019Article
- Activated Fibroblast Program Orchestrates Tumor Initiation and Progression; Molecular Mechanisms and the Associated Therapeutic Strategies.International journal of molecular sciences · 2019Review
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
Metabolic reprogramming is a hallmark of cancer, but most studies focus on the molecular alterations in cancer cells and much less is known on the role of cancer metabolism, from a holistic perspective, for tumor initiation and progression. Increasing epidemiological evidence highlights the tremendous impact that cancer progression has on the host metabolism, especially in cachexia. However, how this benefits the tumor still is not completely understood. Here we review current studies on fatty acid oxidation in tumor cells as a potential therapeutic target in cancer, and how the redistribution of lipids from fat reservoirs to the cancer cell in the micro- and macro-environment impacts tumorigenesis by helping the tumor fulfill its energetic demands at the expense of fat. In this context, we also discuss the critical role of the signaling adaptor p62/Sequestosome 1(SQSTM1) in adipocytes in mediating tumor-induced fat reprograming and the feedback of adipose tissue on tumor aggressiveness via osteopontin and its potential implications in obesity-promoted cancer and fat cachexia. Collectively these studies highlight the importance of the symbiotic collaboration between adipose tissue and tumor to modulate the cancer metabolic fitness.
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.