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Targeting Tumor Microenvironment as a Novel Promising Approach in Adrenal...
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Targeting Tumor Microenvironment as a Novel Promising Approach in Adrenal Tumors

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: closed (25 February 2023) | Viewed by 8983

Special Issue Editors

Prof. Dr. Michaela Luconi

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Guest Editor
Department of Experimental and Clinical Biomedical Sciences, Endocrinology Unit, University of Florence, I‐50139 Florence, Italy
Interests: adrenal tumors; molecular and cell biology of endocrine tumors and metabolic pathologies
Dr. Giulia Cantini

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Guest Editor
Department of Experimental and Clinical Biomedical Sciences, Endocrinology Unit, University of Florence, Florence, Italy
Interests: adrenal tumors; molecular and cell biology of adrenocortical carcinoma; adipose microenvironment
Prof. Dr. Matthias Kroiss

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Guest Editor
1. University Hospital Munich, Ludwig Maximilians-Universität München, München, Germany
2. University Hospital Würzburg and Comprehensive Cancer Center Mainfranken, University of Würzburg, Germany
Interests: adrenal tumors

Special Issue Information

Dear Colleagues,

The recently emerging concept of the tumor microenvironment (TME) is radically changing the way of studying and addressing solid tumors. The TME consists of the complex and dynamic system of cells, soluble factors, matrix factors, and vasculature that form the niche where the tumor grows. The strict reciprocal interaction established between tumor cells and their microenvironment controls tumor development and progression. The complex nature of the adrenal gland structure significantly impacts the different types of tumors that interest this endocrine organ, namely benign and malignant neoplasia of the steroidogenic cortex (adrenocortical adenoma ACA and carcinoma ACC, respectively) and of the catecholamine producing medulla (pheochromocytoma PGL). The variety of hormonal production of the gland in pathophysiological conditions further modulates TME in adrenal tumors, in particular contributing to the immune escape condition of the tumor. The unsatisfactory results of the disease control so far obtained by pharmacological approaches in particular in the adrenal malignancies may be caused by focusing on tumor cells only, neglecting the role of TME in controlling tumor progression and local immune response, as further confirmed by the questionable effects achieved with immunotherapy.

This Special Issue will focus on the aspects of the unique tumor microenvironment characterizing adrenal tumors. A better understanding of the tumor microenvironment characteristics and of the complex crosstalk with the tumor itself will open novel opportunities to develop more effective and personalized therapies for adrenal tumors targeting the disease in the complexity of tumor–TME interaction.

Preclinical and clinical research articles are welcome, as well as reviews and pilot studies focused on cell biology, genetics, molecular mechanisms, diagnostic tools, in vitro and animal models, management, clinics, and therapies addressing the involvement of tumor microenvironment in adrenal tumors, including adrenocortical adenoma, carcinoma, and pheochromocytoma.

Prof. Dr. Michaela Luconi
Dr. Giulia Cantini
Prof. Dr. Matthias Kroiss
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 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. Cancers 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 2900 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

  • adrenal tumors
  • adrenocortical adenomas
  • adrenocortical carcinomas
  • pheochromocytomas
  • glucocorticoids
  • immunotherapy
  • cancer-associated fibroblasts (CAF), adipose cells (CAA), macrophages (CAM)
  • tumor-infiltrating lymphocytes (TIL)
  • genetic/epigenetic landscape

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Published Papers (3 papers)

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Research

22 pages, 13584 KiB  
Article
Targeting Oncogenic Wnt/β-Catenin Signaling in Adrenocortical Carcinoma Disrupts ECM Expression and Impairs Tumor Growth
by Morgan K. Penny, Antonio M. Lerario, Kaitlin J. Basham, Sahiti Chukkapalli, Dipika R. Mohan, Chris LaPensee, Kimber Converso-Baran, Mark J. Hoenerhoff, Laura Suárez-Fernández, Carmen González del Rey, Thomas J. Giordano, Ruolan Han, Erika A. Newman and Gary D. Hammer
Cancers 2023, 15(14), 3559; https://doi.org/10.3390/cancers15143559 - 10 Jul 2023
Cited by 11 | Viewed by 2649
Abstract
Adrenocortical carcinoma (ACC) is a rare but highly aggressive cancer with limited treatment options and poor survival for patients with advanced disease. An improved understanding of the transcriptional programs engaged in ACC will help direct rational, targeted therapies. Whereas activating mutations in Wnt/β-catenin [...] Read more.
Adrenocortical carcinoma (ACC) is a rare but highly aggressive cancer with limited treatment options and poor survival for patients with advanced disease. An improved understanding of the transcriptional programs engaged in ACC will help direct rational, targeted therapies. Whereas activating mutations in Wnt/β-catenin signaling are frequently observed, the β-catenin-dependent transcriptional targets that promote tumor progression are poorly understood. To address this question, we analyzed ACC transcriptome data and identified a novel Wnt/β-catenin-associated signature in ACC enriched for the extracellular matrix (ECM) and predictive of poor survival. This suggested an oncogenic role for Wnt/β-catenin in regulating the ACC microenvironment. We further investigated the minor fibrillar collagen, collagen XI alpha 1 (COL11A1), and found that COL11A1 expression originates specifically from cancer cells and is strongly correlated with both Wnt/β-catenin activation and poor patient survival. Inhibition of constitutively active Wnt/β-catenin signaling in the human ACC cell line, NCI-H295R, significantly reduced the expression of COL11A1 and other ECM components and decreased cancer cell viability. To investigate the preclinical potential of Wnt/β-catenin inhibition in the adrenal microenvironment, we developed a minimally invasive orthotopic xenograft model of ACC and demonstrated that treatment with the newly developed Wnt/β-catenin:TBL1 inhibitor Tegavivint significantly reduced tumor growth. Together, our data support that the inhibition of aberrantly active Wnt/β-catenin disrupts transcriptional reprogramming of the microenvironment and reduces ACC growth and survival. Furthermore, this β-catenin-dependent oncogenic program can be therapeutically targeted with a newly developed Wnt/β-catenin inhibitor. These results show promise for the further clinical development of Wnt/β-catenin inhibitors in ACC and unveil a novel Wnt/β-catenin-regulated transcriptome. Full article
(This article belongs to the Special Issue Targeting Tumor Microenvironment as a Novel Promising Approach in Adrenal Tumors)
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18 pages, 4832 KiB  
Article
The Vault Complex Is Significantly Involved in Therapeutic Responsiveness of Endocrine Tumors and Linked to Autophagy under Chemotherapeutic Conditions
by Stefan Bornstein, Igor Shapiro, Alekhya Mazumdar, Kathrin Zitzmann, Svenja Nölting, Edlira Luca, Felix Beuschlein, Ashish Sharma and Constanze Hantel
Cancers 2023, 15(6), 1783; https://doi.org/10.3390/cancers15061783 - 15 Mar 2023
Cited by 3 | Viewed by 2797
Abstract
Cancers display dynamic interactions with their complex microenvironments that influence tumor growth, invasiveness, and immune evasion, thereby also influencing potential resistance to therapeutic treatments. The tumor microenvironment (TME) includes cells of the immune system, the extracellular matrix, blood vessels, and other cell types, [...] Read more.
Cancers display dynamic interactions with their complex microenvironments that influence tumor growth, invasiveness, and immune evasion, thereby also influencing potential resistance to therapeutic treatments. The tumor microenvironment (TME) includes cells of the immune system, the extracellular matrix, blood vessels, and other cell types, such as fibroblasts or adipocytes. Various cell types forming this TME secrete exosomes, and molecules thereby released into the TME have been shown to be important mediators of cellular communication and interplay. Specific stressors in the TME, such as hypoxia, starvation, inflammation, and damage, can furthermore induce autophagy, a fundamental cellular process that degrades and recycles molecules and subcellular components, and recently it has been demonstrated that the small non-coding vault RNA1-1 plays a role as a regulator of autophagy and the coordinated lysosomal expression and regulation (CLEAR) network. Here, we demonstrate for the first time that intra-tumoral damage following effective therapeutic treatment is linked to specific intracellular synthesis and subsequent exosomal release of vault RNAs in endocrine tumors in vitro and in vivo. While we observed a subsequent upregulation of autophagic markers under classical chemotherapeutic conditions, a downregulation of autophagy could be detected under conditions strongly involving inflammatory cascades. Full article
(This article belongs to the Special Issue Targeting Tumor Microenvironment as a Novel Promising Approach in Adrenal Tumors)
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17 pages, 4463 KiB  
Article
Metformin Treatment Induces Different Response in Pheochromocytoma/Paraganglioma Tumour Cells and in Primary Fibroblasts
by Serena Martinelli, Francesca Amore, Tommaso Mello, Massimo Mannelli, Mario Maggi and Elena Rapizzi
Cancers 2022, 14(14), 3471; https://doi.org/10.3390/cancers14143471 - 17 Jul 2022
Cited by 7 | Viewed by 2435
Abstract
Pheochromocytoma/paragangliomas (PPGLs) are neuroendocrine tumours, often non-metastatic, but without available effective treatment for their metastatic form. Recent studies have shown that metformin exhibits antiproliferative activity in many human cancers, including PPGLs. Nevertheless, no data are available on the role of metformin on PPGL [...] Read more.
Pheochromocytoma/paragangliomas (PPGLs) are neuroendocrine tumours, often non-metastatic, but without available effective treatment for their metastatic form. Recent studies have shown that metformin exhibits antiproliferative activity in many human cancers, including PPGLs. Nevertheless, no data are available on the role of metformin on PPGL cells (two-dimension, 2D) and spheroids (three-dimension, 3D) migration/invasion. In this study, we observed that metformin exerts an antiproliferative effect on 2D and 3D cultures of pheochromocytoma mouse tumour tissue (MTT), either silenced or not for the SDHB subunit. However, metformin did not affect MTT migration. On the other hand, metformin did not have a short-term effect on the proliferation of mouse primary fibroblasts, but significantly decreased their ability to migrate. Although the metabolic changes induced by metformin were similar between MTT and fibroblasts (i.e., an overall decrease of ATP production and an increase in intracellular lactate concentration) the activated signalling pathways were different. Indeed, after metformin administration, MTT showed a reduced phosphorylation of Akt and Erk1/2, while fibroblasts exhibited a downregulation of N-Cadherin and an upregulation of E-Cadherin. Herein, we demonstrated that metformin has different effects on cell growth and spread depending on the cell type nature, underlining the importance of the tumour microenvironment in dictating the drug response. Full article
(This article belongs to the Special Issue Targeting Tumor Microenvironment as a Novel Promising Approach in Adrenal Tumors)
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