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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 3401

Special Issue Editor


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Guest Editor
Department of Molecular and Cellular Biochemistry, College of Medicine, University of Kentucky, Lexington, KY, USA
Interests: integrin signaling; cell motility; invasion; epigenetics; DNA repair; cytoskeletal dynamics

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

Manuscript Submission Information

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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

Published Papers (1 paper)

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Research

17 pages, 7678 KiB  
Article
ITGB6-Knockout Suppresses Cholangiocarcinoma Cell Migration and Invasion with Declining PODXL2 Expression
by Yurie Soejima, Miho Takeuchi, Nao Miyamoto, Motoji Sawabe and Toshio Fukusato
Int. J. Mol. Sci. 2021, 22(12), 6303; https://doi.org/10.3390/ijms22126303 - 11 Jun 2021
Cited by 7 | Viewed by 2899
Abstract
Intrahepatic cholangiocarcinoma (iCCA) is a heterogeneous bile duct cancer with a poor prognosis. Integrin αvβ6 (β6) has been shown to be upregulated in iCCA and is associated with its subclassification and clinicopathological features. In the present study, two ITGB6-knockout HuCCT1 CCA cell [...] Read more.
Intrahepatic cholangiocarcinoma (iCCA) is a heterogeneous bile duct cancer with a poor prognosis. Integrin αvβ6 (β6) has been shown to be upregulated in iCCA and is associated with its subclassification and clinicopathological features. In the present study, two ITGB6-knockout HuCCT1 CCA cell lines (ITGB6-ko cells) were established using the clustered regulatory interspaced short palindromic repeats (CRISPR), an associated nuclease 9 (Cas9) system, and single-cell cloning. RNA sequencing analysis, real-time polymerase chain reaction (PCR), and immunofluorescent methods were applied to explore possible downstream factors. ITGB6-ko cells showed significantly decreased expression of integrin β6 on flow cytometric analysis. Both cell lines exhibited significant inhibition of cell migration and invasion, decreased wound-healing capability, decreased colony formation ability, and cell cycle dysregulation. RNA sequencing and real-time PCR analysis revealed a remarkable decrease in podocalyxin-like protein 2 (PODXL2) expression in ITGB6-ko cells. Colocalization of PODXL2 and integrin β6 was also observed. S100 calcium-binding protein P and mucin 1, which are associated with CCA subclassification, were downregulated in ITGB6-ko cells. These results describe the successful generation of ITGB6-ko CCA cell clones with decreased migration and invasion and downregulation of PODXL2, suggesting the utility of integrin β6 as a possible therapeutic target or diagnostic marker candidate. Full article
(This article belongs to the Special Issue Integrin Signalling in Cancer)
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