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Cells
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Interleukins in Pathogenesis, Progression, and Therapy of Solid Tumors
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Interleukins in Pathogenesis, Progression, and Therapy of Solid Tumors

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Microenvironment".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 4708

Special Issue Editors

Prof. Dr. Malgorzata Krzystek-Korpacka

E-Mail Website
Guest Editor
Department of Medical Biochemistry and Immunochemistry, Wroclaw Medical University, ul. Chałubińskiego 10, 50-368 Wrocław, Poland
Interests: gastrointestinal cancers; inflammation; tumor microenvironment; metabolic reprogramming; inflammatory-bowel disease; gut microbiota
Dr. Katarzyna Neubauer

E-Mail Website
Guest Editor
Department of Gastroenterology and Hepatology, Wroclaw Medical University, Borowska Street 213, 50-556 Wrocław, Poland
Interests: inflammatory bowel disease; ulcerative colitis; Crohn’s disease; diverticular disease; colorectal cancer; biomarkers
Special Issues, Collections and Topics in MDPI journals
Dr. Iwona Bednarz-Misa

E-Mail Website
Guest Editor
Department of Medical Biochemistry and Immunochemistry, Wroclaw Medical University, ul. Chałubińskiego 10, 50-368 Wrocław, Poland
Interests: gastrointestinal cancers; inflammation; tumor microenvironment; inflammatory-bowel disease; Gram-negative bacteria; outer membrane protein

Special Issue Information

Dear Colleagues,

The past few decades have seen numerous trials to exploit an interplay between interleukins and cancer in therapy. However, interleukin-based approaches have so far been not only disappointingly ineffective but even toxic.

This Special Issue welcomes review articles and original reports improving our understanding of the complex role played by interleukins in cancer pathogenesis and progression and orchestration of the tumor microenvironment, unraveling the molecular mechanisms involved in transducing signals conveyed by interleukins and exploring them as potential therapeutics or molecular targets in anti-neoplastic strategies.

Prof. Dr. Malgorzata Krzystek-Korpacka
Dr. Katarzyna Neubauer
Dr. Iwona Bednarz-Misa
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • immunosurveillance
  • immunotherapy
  • immunosuppression
  • tumor microenvironment
  • neoplastic transformation
  • metabolic reprogramming

Published Papers (1 paper)

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Research

18 pages, 3113 KiB  
Article
Targeting the gp130/STAT3 Axis Attenuates Tumor Microenvironment Mediated Chemoresistance in Group 3 Medulloblastoma Cells
by Lakshana Sreenivasan, Ling Vicky Li, Pascal Leclair and Chinten James Lim
Cells 2022, 11(3), 381; https://doi.org/10.3390/cells11030381 - 23 Jan 2022
Cited by 8 | Viewed by 4334
Abstract
Medulloblastoma (MB) is the most common malignant pediatric brain tumor. Of the four molecular subgroups, Group 3 MB is the most aggressive and has the worst prognosis. To understand the origins of chemoresistance involving IL-6/STAT3 signaling, we used in vitro co-culture systems to [...] Read more.
Medulloblastoma (MB) is the most common malignant pediatric brain tumor. Of the four molecular subgroups, Group 3 MB is the most aggressive and has the worst prognosis. To understand the origins of chemoresistance involving IL-6/STAT3 signaling, we used in vitro co-culture systems to investigate the contribution of microglia as a brain tumor microenvironment cellular source of paracrine cytokines that promotes acquired drug resistance in Group 3 MB. MB cells subjected to co-culture with microglia exhibited increased expression of phosphorylated JAK1 and STAT3, which was correlated with enhanced resistance to vincristine. We found that both microglia and MB cells co-cultured with microglia secreted significant quantities of IL-6, indicating that IL-6 is a paracrine and autocrine cytokine able to initiate and sustain STAT3 activity in MB cells. Surprisingly, IL-6R−/− MB cells, which cannot respond to exogenous IL-6 stimuli, were responsive to microglia co-culture induced activation of STAT3 and chemoresistance. Subsequently, we found that MB cells conditioned in vitro with the IL-6 family cytokines, IL-6, OSM, LIF, or IL-11, exhibited enhanced JAK1/STAT3 activity and chemoresistance. Intriguingly, MB cells conditioned with any one of the IL-6 family cytokine secreted multiple IL-6 family cytokines, implicating a feedback network involving multiple cytokines. The IL-6 family cytokine receptors share a common signal transducing β-subunit, gp130, which may be targeted to mitigate tumor chemoresistance. We showed that microglia co-culture failed to induce chemoresistance of gp130−/− MB cells, and that combination treatment using gp130 inhibitors, or with the JAK inhibitor ruxolitinib, effectively overcame the observed resistance to vincristine in gp130 expressing MB cells. Our in vitro studies highlight the gp130/JAK/STAT pathway as a therapeutic target in combating acquired treatment resistance in Group 3 MB. Full article
(This article belongs to the Special Issue Interleukins in Pathogenesis, Progression, and Therapy of Solid Tumors)
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