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Cancers
Special Issues
Intercellular Communication between Tumor and Stromal Cells in Endocrine-Related Cancer
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Intercellular Communication between Tumor and Stromal Cells in Endocrine-Related Cancer

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 7266

Special Issue Editors

Prof. Dr. Takashi Suzuki

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Guest Editor
Department of Anatomic Pathology, Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Miyagi-ken, Japan
Interests: endocrine-related tumor; enzyme; hormone action; pathology; receptor
Special Issues, Collections and Topics in MDPI journals
Dr. Yasuhiro Miki

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Guest Editor
Department of Anatomic Pathology, Tohoku University Graduate School of Medicine 2-1 Seiryo-cho, Aoba-ku, Sendai 981-8575, Miyagi, Japan
Interests: breast cancer; endometrial cancer; tumor microenvironment; intracrine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

The tumor microenvironment is composed not only of tumor cells but also contains various stromal cells including leukocytes, macrophages, fibroblasts, and endothelium, which, together with cross‑talks between tumor cells and other cellular components, is strongly associated with tumor progression. Importantly, immune checkpoint inhibitors are currently regarded as a promising therapeutic strategy for some cancers.

Endocrine-related cancers (i.e., breast, endometrial, prostate cancers, etc.) are a common malignant neoplasm worldwide. Biologically active steroids, such as estrogen and androgen, are locally produced and act in cancer tissues, and hormone therapies are used in these patients. Recent emerging evidence suggests that the tumor microenvironment is greatly affected by hormonal actions, which sheds new light on the pathogenesis and therapeutic strategy in endocrine-related cancers.

This Special Issue will therefore be reviewed by experts in this field and encompass new research articles and timely reviews regarding the tumor microenvironment in endocrine-related cancers.

Prof. Dr. Takashi Suzuki
Dr. Yasuhiro Miki
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.

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Published Papers (3 papers)

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Research

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20 pages, 3126 KiB  
Article
The Pro-Tumorigenic Role of Chemotherapy-Induced Extracellular HSP70 from Breast Cancer Cells via Intratumoral Macrophages
by Mio Yamaguchi-Tanaka, Kiyoshi Takagi, Yasuhiro Miki, Ai Sato, Erina Iwabuchi, Minoru Miyashita and Takashi Suzuki
Cancers 2023, 15(6), 1903; https://doi.org/10.3390/cancers15061903 - 22 Mar 2023
Cited by 8 | Viewed by 2256
Abstract
Tumor-associated macrophages (TAMs) contribute to tumor progression and chemoresistance; it is therefore important to clarify the altered functions of macrophages following chemotherapy. While extracellular heat shock protein (HSP) 70 is associated with therapeutic resistance, the effects of HSP70 on TAMs remain largely unknown. [...] Read more.
Tumor-associated macrophages (TAMs) contribute to tumor progression and chemoresistance; it is therefore important to clarify the altered functions of macrophages following chemotherapy. While extracellular heat shock protein (HSP) 70 is associated with therapeutic resistance, the effects of HSP70 on TAMs remain largely unknown. Here, we conducted in vitro experiments and immunohistochemistry in 116 breast carcinoma specimens to determine whether the secretion of HSP70 from breast cancer cells following chemotherapy affects macrophage function. It was revealed that the interaction of epirubicin (EPI)-exposed breast cancer cells with macrophages enhanced tumor progression, and EPI promoted the secretion of extracellular HSP70 from breast cancer cells. The expression of pro-tumorigenic macrophage marker CD163 was decreased in macrophages treated with a conditioned medium (CM) from HSP70-silenced breast cancer cells. Breast cancer cells treated with CM from HSP70-silenced breast cancer cells showed decreased expression of transforming growth factor (TGF)-β, and the pro-tumorigenic effects of macrophages were impaired when TGF-β signaling was inhibited. Immunohistochemistry demonstrated that HSP70 served as a poor prognostic factor in conjunction with macrophage infiltration. It was therefore concluded that extracellular HSP70 levels increased following chemotherapy and enhanced the pro-tumorigenic effects of TAMs, either directly or indirectly, by regulating TGF-β expression in breast cancer cells. Full article
(This article belongs to the Special Issue Intercellular Communication between Tumor and Stromal Cells in Endocrine-Related Cancer)
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17 pages, 3293 KiB  
Article
Estrogen Receptor β (ESR2) Transcriptome and Chromatin Binding in a Mantle Cell Lymphoma Tumor Model Reveal the Tumor-Suppressing Mechanisms of Estrogens
by Dan Huang, Zhiqiang Huang, Rajitha Indukuri, Chandrashekar Bangalore Revanna, Mattias Berglund, Jiyu Guan, Konstantin Yakimchuk, Anastasios Damdimopoulos, Cecilia Williams and Sam Okret
Cancers 2022, 14(13), 3098; https://doi.org/10.3390/cancers14133098 - 24 Jun 2022
Cited by 2 | Viewed by 2434
Abstract
Mantle cell lymphoma (MCL) is a non-Hodgkin lymphoma with one of the highest male-to-female incidence ratios. The reason for this is not clear, but epidemiological as well as experimental data have suggested a role for estrogens, particularly acting through estrogen receptor β (ESR2). [...] Read more.
Mantle cell lymphoma (MCL) is a non-Hodgkin lymphoma with one of the highest male-to-female incidence ratios. The reason for this is not clear, but epidemiological as well as experimental data have suggested a role for estrogens, particularly acting through estrogen receptor β (ESR2). To study the ESR2 effects on MCL progression, MCL cells sensitive and resistant to the Bruton tyrosine kinase inhibitor ibrutinib were grafted to mice and treated with the ESR2-selective agonist diarylpropionitrile (DPN). The results showed that the DPN treatment of mice grafted with both ibrutinib-sensitive and -resistant MCL tumors resulted in impaired tumor progression. To identify the signaling pathways involved in the impaired tumor progression following ESR2 agonist treatment, the transcriptome and ESR2 binding to target genes were investigated by genome-wide chromatin immunoprecipitation in Granta-519 MCL tumors. DPN-regulated genes were enriched in several biological processes that included cell–cell adhesion, endothelial–mesenchymal transition, nuclear factor-kappaB signaling, vasculogenesis, lymphocyte proliferation, and apoptosis. In addition, downregulation of individual genes, such as SOX11 and MALAT1, that play a role in MCL progression was also observed. Furthermore, the data suggested an interplay between the lymphoma cells and the tumor microenvironment in response to the ESR2 agonist. In conclusion, the results clarify the mechanisms by which estrogens, via ESR2, impair MCL tumor progression and provide a possible explanation for the sex-dependent difference in incidence. Furthermore, targeting ESR2 with a selective agonist may be an additional option when considering the treatment of both ibrutinib-sensitive and -resistant MCL tumors. Full article
(This article belongs to the Special Issue Intercellular Communication between Tumor and Stromal Cells in Endocrine-Related Cancer)
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Review

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18 pages, 1761 KiB  
Review
New Perspectives on Sex Steroid Hormones Signaling in Cancer-Associated Fibroblasts of Non-Small Cell Lung Cancer
by Chihiro Inoue, Yasuhiro Miki and Takashi Suzuki
Cancers 2023, 15(14), 3620; https://doi.org/10.3390/cancers15143620 - 14 Jul 2023
Cited by 2 | Viewed by 1954
Abstract
The importance of sex hormones, especially estrogen, in the pathogenesis of non-small-cell lung cancer (NSCLC) has attracted attention due to its high incidence among young adults and nonsmokers, especially those who are female. Cancer-associated fibroblasts (CAFs) reside in the cancer stroma and influence [...] Read more.
The importance of sex hormones, especially estrogen, in the pathogenesis of non-small-cell lung cancer (NSCLC) has attracted attention due to its high incidence among young adults and nonsmokers, especially those who are female. Cancer-associated fibroblasts (CAFs) reside in the cancer stroma and influence cancer growth, invasion, metastasis, and acquisition of drug resistance through interactions with cancer cells and other microenvironmental components. Hormone-mediated cell–cell interactions are classic cell–cell interactions and well-known phenomena in breast cancer and prostate cancer CAFs. In cancers of other organs, including NSCLC, the effects of CAFs on hormone-receptor expression and hormone production in cancer tissues have been reported; however, there are few such studies. Many more studies have been performed on breast and prostate cancers. Recent advances in technology, particularly single-cell analysis techniques, have led to significant advances in the classification and function of CAFs. However, the importance of sex hormones in cell–cell interactions of CAFs in NSCLC remains unclear. This review summarizes reports on CAFs in NSCLC and sex hormones in cancer and immune cells surrounding CAFs. Furthermore, we discuss the prospects of sex-hormone research involving CAFs in NSCLC. Full article
(This article belongs to the Special Issue Intercellular Communication between Tumor and Stromal Cells in Endocrine-Related Cancer)
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