AI Article Synopsis
- Apolipoproteins (APOs) play a significant role in lipid metabolism and have been studied more in cardiovascular diseases than in cancer, but recent research is changing that.
- Studies show that APOs interact with key pathways involved in tumor development, and their imbalance could be used as biomarkers for diagnosing and tracking cancer.
- The review highlights the mechanisms by which APOs contribute to cancer, their potential as biomarkers, genetic variations affecting cancer risk, and the prospects for using APOs in anti-cancer therapies.
Article Abstract
Apolipoproteins (APOs), the primary protein moiety of lipoproteins, are known for their crucial role in lipid traffic and metabolism. Despite extensive exploration of APOs in cardiovascular diseases, their roles in cancers did not attract enough attention. Recently, research focusing on the roles of APOs in cancers has flourished. Multiple studies demonstrate the interaction of APOs with classical pathways of tumorigenesis. Besides, the dysregulation of APOs may indicate cancer occurrence and progression, thus serving as potential biomarkers for cancer patients. Herein, we summarize the mechanisms of APOs involved in the development of various cancers, their applications as cancer biomarkers and their genetic polymorphism associated with cancer risk. Additionally, we also discuss the potential anti-cancer therapies by virtue of APOs. The comprehensive review of APOs in cancers may advance the understanding of the roles of APOs in cancers and their potential mechanisms. We hope that it will provide novel clues and new therapeutic strategies for cancers.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9732396 | PMC |
| http://dx.doi.org/10.3389/fphar.2022.1051280 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Single-cell RNA sequencing identifies CXADR as a fate determinant of the placental exchange surface.
Nat Commun
January 2025
Department of Obstetrics and Gynaecology, University of Cambridge, NIHR Cambridge Biomedical Research Centre, Cambridge, United Kingdom.
The placenta is the critical interface between mother and fetus, and consequently, placental dysfunction underlies many pregnancy complications. Placental formation requires an adequate expansion of trophoblast stem and progenitor cells followed by finely tuned lineage specification events. Here, using single-cell RNA sequencing of mouse trophoblast stem cells during the earliest phases of differentiation, we identify gatekeepers of the stem cell state, notably Nicol1, and uncover unsuspected trajectories of cell lineage diversification as well as regulators of lineage entry points.
View Article and Find Full Text PDFLung Adenocarcinoma and Peripheral Blood Eosinophilia.
Cureus
November 2024
Medical Oncology, Hospital Professor Doutor Fernando Fonseca, Lisbon, PRT.
There are many causes of peripheral blood eosinophilia (PBE), including allergic, infectious, rheumatic, and hematologic disorders. Solid tumor cancers, such as lung cancer, can also cause PBE, and although rare, being diagnosed with PBE in this way is associated with a worse prognosis than for lung cancer patients without PBE. Additionally, some cancer patients develop PBE when receiving treatment with immune checkpoint inhibitors (ICIs).
View Article and Find Full Text PDFpERK transition-induced directional mode switching promotes epithelial tumor cell migration.
Proc Natl Acad Sci U S A
December 2024
Shenzhen Key Laboratory of Metabolism and Cardiovascular Homeostasis, Shenzhen University Medical School, Shenzhen University, Shenzhen, Guangdong 518055, China.
Increasing evidence suggests that tumor cells exhibit extreme plasticity in migration modes in order to adapt to microenvironments. However, the underlying mechanism for governing the migration mode switching is still unclear. Here, we revealed that epithelial tumor cells could develop a stable directional mode driven by hyperactivated ERK activity.
View Article and Find Full Text PDFLoss of NUMB drives aggressive bladder cancer via a RHOA/ROCK/YAP signaling axis.
Nat Commun
December 2024
European Institute of Oncology IRCCS, Milan, Italy.
Advances in bladder cancer (BCa) treatment have been hampered by the lack of predictive biomarkers and targeted therapies. Here, we demonstrate that loss of the tumor suppressor NUMB promotes aggressive bladder tumorigenesis and worsens disease outcomes. Retrospective cohort studies show that NUMB-loss correlates with poor prognosis in post-cystectomy muscle-invasive BCa patients and increased risk of muscle invasion progression in non-muscle invasive BCa patients.
View Article and Find Full Text PDFTumor-derived miR-9-5p-loaded EVs regulate cholesterol homeostasis to promote breast cancer liver metastasis in mice.
Nat Commun
December 2024
Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Wuhan University, Wuhan, Hubei, 430072, China.
Cancer cells secrete extracellular vesicles (EV) encapsulating bioactive cargoes to facilitate inter-organ communication in vivo and are emerging as critical mediators of tumor progression and metastasis, a condition which is often accompanied by a dysregulated cholesterol metabolism. Whether EVs are involved in the control of cholesterol homeostasis during tumor metastasis is still undefined and warrant further investigation. Here, we find that breast cancer-derived exosomal miR-9-5p induces the expression of HMGCR and CH25H, two enzymes involved in cholesterol synthesis and the conversion of 25-hydroxycholesterol from cholesterol by targeting INSIG1, INSIG2 and ATF3 genes in the liver.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!