Integrin Signalling in Cancer
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".
Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 4261
Special Issue Editor
Special Issue Information
Dear Colleagues,
Comprised of 24 members, the integrin family members serve as receptors for various extracellular matrices that allow cells to adhere, create complex structures, and sense their environment. Originally named for their ability to integrate these extracellular signals to the cell’s interior, integrins are responsible for amplifying and potentiating signals from growth factors and other extracellular stimuli that are critical for normal physiology. In fact, there are few, if any, physiological processes that are not influenced by integrin signaling in multicellular organisms. During malignant progression, tumor cells evolve complex interactions with their microenvironment, mediated in large part by integrins that influence progression and define the biology of the tumor. Dissecting the signaling pathways altered by integrin has given and will continue to contribute great insight into the processes that perpetuate a malignant phenotype. As our knowledge of cancer biology increases, so expands the variety of mechanisms we recognize that integrins influence that provide critical insight that may guide how new targeted therapies are devised.
The purpose of this Special Issue is to highlight current research on various and unique aspects of integrin signaling and how this contextual signaling impacts cancer biology including cell motility and invasion, stem cell properties, anoikis, cell proliferation, angiogenesis, metabolism, metastasis, and other important hallmarks of cancer.
Prof. Kathleen L. O'Connor
Guest Editor
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Keywords
- Integrin
- Cytoskeleton
- Cell motility
- Invasion
- Metastasis
- Anoikis
- Apoptosis
- Cell proliferation
- Therapeutic resistance
- Cancer stem cell
- Signal transduction
- Mechanotransduction
- Transcription
- Epigenetics
- Tumor suppressor
- Oncogene
- Microenvironment
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