ArticleAging2024
ITGB2 fosters the cancerous characteristics of ovarian cancer cells through its role in mitochondrial glycolysis transformation.
Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
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Who cites it
5 citing papers in PubMed, 2 citations in OpenAlex.
- Whole ovary cryopreservation and transplantation: a narrative review of technological advances, biological hurdles, and clinical translation in fertility preservation.Journal of assisted reproduction and genetics · 2026Review
- Immune heterogeneity and therapeutic resistance in gynecological malignancies.Frontiers in immunology · 2026Review
- Targeting the tumor cell-intrinsic ITGB2 axis inhibits melanoma progression.Molecular cancer · 2025Article
- Screening and Functional Transformation Analysis of Genes Related to Skeletal Muscle Development in Supplemental-Fed Oula Sheep.Animals : an open access journal from MDPI · 2025Article
- KLC3 activates PI3K/AKT signaling and promotes ovarian cancer cell proliferation and migration through COL3A1.Oncology reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Related studies have shown that ITGB2 mediates mitochondrial glycolytic transformation in cancer-associated fibroblasts and participates in tumor occurrence, metastasis and invasion of cancer cells. Based on these studies, we tried to construct a mitochondrial glycolysis regulatory network and explored its effect on mitochondrial homeostasis and ovarian cancer cells' cancerous characteristics. Our research revealed a distinct increase in the expression of ITGB2 and associated signaling pathway elements (PI3K-AKT-mTOR) in cases of ovarian cancer. ITGB2 might control mTOR expression via the PI3K-AKT pathway, thus promote mitochondrial glycolysis transformation and cell energy supply in ovarian cancer. This pathway could also inhibit mitophagy, maintain mitochondrial stability, and enhance the cancerous characteristics in case of ovarian cancer cells by mediating mitochondrial glycolytic transformation. Thus, we concluded that ITGB2-associated signaling route (PI3K-AKT-mTOR) may contribute to the progression of cancerous traits in ovarian cancer via mediating mitochondrial glycolytic transformation.
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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.