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Hormones and Tumors

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A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 555

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Special Issue Editors

Prof. Dr. Kiyoshi Takagi

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Guest Editor

Department of Pathology and Histotechnology, Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Miyagi-ken, Japan
Interests: breast cancer; chemoresistance; molecular biology; prostate cancer; tumor microenvironment

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
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Special Issue Information

Dear Colleagues,

It is well known that hormones contribute immensely not only to normal tissue/cell functions but also to the development of various disorders. Tumors arising from endocrine organs and neuroendocrine neoplasms produce active hormones and cause various clinical symptoms. Endocrine-related cancers such as breast and prostate cancers are common malignant neoplasms worldwide, and hormones are locally produced and act in cancer tissues. In recent years, new techniques have been developed to visualize hormonal dynamics, and new light is being shed on the diagnosis of endocrine-related tumors. Moreover, a detailed investigation of hormonal actions will lead to the development of a new therapeutic strategy for endocrine-related tumors. This Special Issue will be reviewed by experts in this field and encompass new research articles and timely reviews regarding hormones and tumors.

Prof. Dr. Kiyoshi Takagi
Prof. Dr. Takashi Suzuki
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

diagnosis
hormone
prognosis
progression
therapy
tumor

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Published Papers (1 paper)

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Research

15 pages, 4754 KiB

Open AccessArticle

Discoidin Domain Receptor 2 Contributes to Breast Cancer Progression and Chemoresistance by Interacting with Collagen Type I

by Ai Sato, Kiyoshi Takagi, Momoka Yoshida, Mio Yamaguchi-Tanaka, Mikoto Sagehashi, Yasuhiro Miki, Minoru Miyashita and Takashi Suzuki

Cancers 2024, 16(24), 4285; https://doi.org/10.3390/cancers16244285 - 23 Dec 2024

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Abstract

Background: Chemoresistance is an important issue to be solved in breast cancer. It is well known that the content and morphology of collagens in tumor tissues are drastically altered following chemotherapy, and discoidin domain receptor 2 (DDR2) is a unique type of receptor tyrosine kinase (RTK). This RTK is activated by collagens, playing important roles in human malignancies. However, the contribution to the chemoresistance of DDR2 in terms of the association with collagens remains largely unclear in breast cancer. Methods: We immunolocalized DDR2 and collagen type I in 224 breast cancer tissues and subsequently conducted in vitro studies to confirm the role of DDR2 in breast cancer chemoresistance using chemosensitive and chemoresistant cell lines. Results: DDR2 immunoreactivity was positively correlated with aggressive behaviors of breast cancer and was significantly associated with an increased risk of recurrence, especially in those who received chemotherapy. Moreover, in vitro experiments demonstrated that DDR2 promoted the proliferative activity of breast cancer cells, and cell viability after epirubicin treatment was significantly maintained by DDR2 in a collagen I-dependent manner. Conclusions: These data suggested that DDR2 could be a poor prognostic factor associated with cell proliferation and chemotherapy resistance in human breast cancer. Full article

(This article belongs to the Special Issue Hormones and Tumors)

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Figure 1

Figure 1
Representative image of DDR2 and collagen type I immunostaining in human breast cancer. (A–C): immunostaining of DDR2 in breast cancer cells (A), normal breast epithelium (B), and human heart as a positive control of DDR2 (C). (D–F): immunostaining of collagen type I in cancerous stroma (D), normal breast stroma (E), and human skin as a positive control of collagen type I (F). Bar = 100 µm, respectively. Full article ">Figure 2
Association between DDR2 status and clinical outcomes of breast cancer patients (n = 224). (A–D): disease-free survival (A,C) and breast cancer-specific survival (B,D) according to DDR2 status (A,B) or DDR2/collagen type I combination status (C,D). (E–H): disease-free survival according to DDR2 status (E,F) or DDR2/collagen type I combination status (G,H) in the patients who received chemotherapy (E,G) or not (F,H). Full article ">Figure 3
The effect of DDR2 in the proliferation of human breast cancer cell lines in the presence of collagen type I. (A) Immunoblotting of exogenous DDR2 protein in MCF-7, MDA-MB-231, and T47D cells. (B–D): cell proliferation of MCF-7 (A), MDA-MB-231 (B), and T47D (D) transfected with an empty vector or DDR2-expressing vector in the absence or presence of collagen coating. (E) Immunoblotting of DDR2 in the cells transfected with siRNA against DDR2 (siDDR2-1, 2). (F–H): cell proliferation of MCF-7 (F), MDA-MB-231 (G), and T47D (H) transfected with siRNAs in the presence of collagen coating. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the empty vector, respectively. Full article ">Figure 4
The effect of DDR2 on the resistance to epirubicin in the breast cancer cell lines. (A–C): viability of MCF-7 (A), MDA-MB-231 (B), and T47D (C) transfected with an empty vector or DDR2-expressing vector under epirubicin treatment (500 nM for MCF-7; 250 nM for MDA-MB-231 and T47D). These cells were plated onto collagen-coated culture plates. * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the empty vector, respectively. (D–F): viability of MCF-7 (D), MDA-MB-231 (E), and T47D (F) transfected with siRNA targeting DDR2 under epirubicin treatment. (G,H) mRNA and protein expression in chemosensitive parental cells and epirubicin-resistant cells (G; MCF-7 series, H; MDA-MB-231 series). ** p < 0.01, respectively. (I,J) The effect of DDR2 inhibitor WRG-28 treatment (48 h) on the proliferation of chemosensitive parental cells and epirubicin-resistant cells (F; MCF-7 series, G; MDA-MB-231 series). Full article ">Figure 5
The effect of DDR2 on the apoptosis of breast MCF-7 (A), MDA-MB-231 (B), and T47D (C). *** p < 0.001. Full article ">

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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Discoidin Domain Receptor 2 contributes to breast cancer progression and chemoresistance by interacting with collagen type I
Authors: Ai Sato; Kiyoshi Takagi; Momoka Yoshida; Mio Yamaguchi-Tanaka; Mikoto Sagehashi; Yasuhiro Miki; Minoru Miyashita; Takashi Suzuki
Affiliation: Department of Pathology and Histotechnology, Tohoku University Graduate School of Medicine, Sendai, Japan
Abstract: Background: Chemoresistance is an important issue to be solved in breast cancer. It is well known that the content and morphology of collagens in tumor tissues are drastically altered following chemotherapy, and discoidin domain receptor 2 (DDR2) is a unique type of receptor tyrosine kinases activated by collagens, playing important roles in human malignancies. However, the contribution to the chemoresistance of DDR2 in terms of the association with collagens remains largely unclear in breast cancer. Methods: We immunolocalized DDR2 and collagen type I in 224 breast cancer tissues and subsequently conducted in vitro studies to confirm the role of DDR2 in breast cancer chemoresistance using chemo-sensitive and chemo-resistant cell lines. Results: DDR2 immunoreactivity was positively correlated with aggressive behaviors of breast cancer and was significantly associated with increased risk of recurrence, especially in those who received chemotherapy. Moreover, in vitro experiments demonstrated that DDR2 promoted the proliferative activity of breast cancer cells, and cell viability was significantly maintained by DDR2 overexpression cells compared to control cells in the presence of Epirubicin. Conclusion: These data suggested that DDR2 could be a poor prognostic factor associated with cell proliferation and chemotherapy resistance in human breast cancer.