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New Advances in Endocrine-Related Cancer 2022
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New Advances in Endocrine-Related Cancer 2022

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (15 February 2023) | Viewed by 9087

Special Issue Editor

Dr. Tae Woo Kim

E-Mail Website
Guest Editor
Department of Biopharmaceutical Engineering, Dongguk University-WISE, Gyeongju, Gyeongbuk 38066, Republic of Korea
Interests: ROS; calcium; ER stress; NOX; apoptosis; cell death; natural products; phytochemicals; plant antioxidants; cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Endocrine-related cancers are classically divided into groups of sex steroid responsive cancers, including prostate cancer, testis cancer, ovary cancer, thyroid cancer, and breast cancer. In endocrine-related cancer therapy, long-term antihormone adjuvant therapeutic strategy has been found to reduce mortality and recurrence; however, its role in acquired resistance is still unclear. The hormones play a potential role, and the relationship between hormone and endocrine-related cancer is important when it comes to studying the mechanism for tumor survival and cell death. Novel or famous antitumor reagents against endocrine-related cancers are a new, advanced strategy to overcome resistance in cancer therapy, but the underlying mechanisms are still not fully clarified. To overcome resistance, several anticancer drugs have been found to potentially induce an antitumor effect through apoptosis, autophagy, necroptosis, cell cycle arrest, angiogenesis, and epigenetics on the tumor microenvironment, including growth factor deprivation, hypoxia, radiation, cancer-related fibroblasts, extracellular matrix (ECM), exosomes, and inflammatory and immune cells.

This Special Issue of IJMS, “New Advances in Endocrine-Related Cancer”, will focus on new, advanced therapeutic strategies to overcome chemoresistance in endocrine-related cancer therapy. Moreover, we will focus on progress in our understanding of endocrine resistance and therapeutic approaches to develop new treatments to improve the therapy of endocrine chemoresistance.

Dr. Tae Woo Kim
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • endocrine-related cancer
  • hormone
  • hypoxia
  • apoptosis
  • autophagy
  • epigenetics
  • cell death
  • cell survival
  • resistance

Published Papers (4 papers)

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Research

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12 pages, 1487 KiB  
Article
The Expression of Autophagy-Associated Genes Represents a Valid Footprint for Aggressive Pancreatic Neuroendocrine Neoplasms
by Sami Matrood, Leander Edwin Melms, Detlef Klaus Bartsch and Pietro Di Fazio
Int. J. Mol. Sci. 2023, 24(4), 3636; https://doi.org/10.3390/ijms24043636 - 11 Feb 2023
Cited by 2 | Viewed by 1429
Abstract
Pancreatic neuroendocrine neoplasms (pNEN) are rare and heterogeneous tumors. Previous investigations have shown that autophagy can be a target for cancer therapy. This study aimed to determine the association between the expression of autophagy-associated gene transcripts and clinical parameters in pNEN. In total, [...] Read more.
Pancreatic neuroendocrine neoplasms (pNEN) are rare and heterogeneous tumors. Previous investigations have shown that autophagy can be a target for cancer therapy. This study aimed to determine the association between the expression of autophagy-associated gene transcripts and clinical parameters in pNEN. In total, 54 pNEN specimens were obtained from our human biobank. The patient characteristics were retrieved from the medical record. RT-qPCR was performed to assess the expression of the autophagic transcripts BECN1, MAP1LC3B, SQSTM1, UVRAG, TFEB, PRKAA1, and PRKAA2 in the pNEN specimens. A Mann–Whitney U test was used to detect differences in the expression of autophagic gene transcripts between different tumor characteristics. This study showed that G1 sporadic pNEN have a higher expression of autophagic genes compared to G2. Lymphatic and distant metastasis occurred significantly more often in pNEN with a decreased expression of the autophagic genes. Within sporadic pNEN, the insulinomas express higher levels of autophagic transcripts than gastrinomas and non-functional pNEN. MEN1-associated pNEN show a higher expression of autophagic genes than sporadic pNEN. In summary, a decreased expression of autophagic transcripts distinguishes metastatic from non-metastatic sporadic pNEN. The significance of autophagy as a molecular marker for prognosis and therapy decisions needs to be further investigated. Full article
(This article belongs to the Special Issue New Advances in Endocrine-Related Cancer 2022)
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18 pages, 30667 KiB  
Article
6-Shogaol Overcomes Gefitinib Resistance via ER Stress in Ovarian Cancer Cells
by Tae Woo Kim and Hee Gu Lee
Int. J. Mol. Sci. 2023, 24(3), 2639; https://doi.org/10.3390/ijms24032639 - 30 Jan 2023
Cited by 5 | Viewed by 2042
Abstract
In women, ovary cancer is already the fifth leading cause of mortality worldwide. The use of cancer therapies, such as surgery, radiotherapy, and chemotherapy, may be a powerful anti-cancer therapeutic strategy; however, these therapies still have many problems, including resistance, toxicity, and side [...] Read more.
In women, ovary cancer is already the fifth leading cause of mortality worldwide. The use of cancer therapies, such as surgery, radiotherapy, and chemotherapy, may be a powerful anti-cancer therapeutic strategy; however, these therapies still have many problems, including resistance, toxicity, and side effects. Therefore, natural herbal medicine has the potential to be used for cancer therapy because of its low toxicity, fewer side effects, and high success. This study aimed to investigate the anti-cancer effect of 6-shogaol in ovarian cancer cells. 6-shogaol induces ER stress and cell death via the reduction in cell viability, the increase in LDH cytotoxicity, caspase-3 activity, and Ca2+ release, and the upregulation of GRP78, p-PERK, p-eIF2α, ATF-4, CHOP, and DR5. Moreover, 6-shogaol treatment medicates endoplasmic reticulum (ER) stress and cell death by upregulating Nox4 and releasing ROS. The knockdown of Nox4 in ovarian cancer cells inhibits ER stress and cell death by blocking the reduction in cell viability and the enhancement of LDH cytotoxicity, caspase-3 activity, Ca2+, and ROS release. In gefitinib-resistant ovarian cancer cells, A2780R and OVCAR-3R, 6-shogaol/gefitinib overcomes gefitinib resistance by inhibiting EMT phenomena such as the reduction in E-cadherin, and the increase in N-cadherin, vimentin, Slug, and Snail. Therefore, our results suggest that 6-shogaol exerts a potential anti-cancer effect in ovarian cancer and combination treatment with 6-shogaol and gefitinib may provide a novel anti-tumor therapeutic strategy in gefitinib-resistant ovarian cancer. Full article
(This article belongs to the Special Issue New Advances in Endocrine-Related Cancer 2022)
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15 pages, 2987 KiB  
Article
Immunomodulation of HDAC Inhibitor Entinostat Potentiates the Anticancer Effects of Radiation and PD-1 Blockade in the Murine Lewis Lung Carcinoma Model
by Yeeun Kim, Kyunghee Park, Yeon Jeong Kim, Sung-Won Shin, Yeon Joo Kim, Changhoon Choi and Jae Myoung Noh
Int. J. Mol. Sci. 2022, 23(24), 15539; https://doi.org/10.3390/ijms232415539 - 8 Dec 2022
Cited by 4 | Viewed by 2287
Abstract
Although the combination of radiotherapy and immunotherapy has proven to be effective in lung cancer treatment, it may not be sufficient to fully activate the antitumor immune response. Here, we investigated whether entinostat, a histone deacetylase inhibitor, could improve the efficacy of radiotherapy [...] Read more.
Although the combination of radiotherapy and immunotherapy has proven to be effective in lung cancer treatment, it may not be sufficient to fully activate the antitumor immune response. Here, we investigated whether entinostat, a histone deacetylase inhibitor, could improve the efficacy of radiotherapy and anti-PD-1 in a murine syngeneic LL/2 tumor model. A total of 12 Gy of X-rays administered in two fractions significantly delayed tumor growth in mice, which was further enhanced by oral entinostat administration. Flow cytometry-aided immune cell profiling revealed that entinostat increased radiation-induced infiltration of myeloid-derived suppressor cells and CD8+ T cells with decreased regulatory T-cells (Tregs). Transcriptomics-based immune phenotype prediction showed that entinostat potentiated radiation-activated pathways, such as JAK/STAT3/interferon-gamma (IFN-γ) and PD-1/PD-L1 signaling. Entinostat augmented the antitumor efficacy of radiation and anti-PD-1, which may be related to an increase in IFN-γ-producing CD8+ T-cells with a decrease in Treg cells. Comparative transcriptomic profiling predicted that entinostat increased the number of dendritic cells, B cells, and T cells in tumors treated with radiation and anti-PD-1 by inducing MHC-II genes. In conclusion, our findings provided insights into how entinostat improves the efficacy of ionizing radiation plus anti-PD-1 therapy and offered clues for developing new strategies for clinical trials. Full article
(This article belongs to the Special Issue New Advances in Endocrine-Related Cancer 2022)
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Review

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19 pages, 1624 KiB  
Review
Cell Component and Function of Tumor Microenvironment in Thyroid Cancer
by Eunah Shin and Ja Seung Koo
Int. J. Mol. Sci. 2022, 23(20), 12578; https://doi.org/10.3390/ijms232012578 - 20 Oct 2022
Cited by 9 | Viewed by 2394
Abstract
Thyroid cancer is the most common cancer in the endocrine system. Most thyroid cancers have good prognosis, but some of them are resistant to treatment or show aggressive behavior. Like other tumors, thyroid cancers harbor tumor microenvironment (TME) composed of cancer associated fibroblasts [...] Read more.
Thyroid cancer is the most common cancer in the endocrine system. Most thyroid cancers have good prognosis, but some of them are resistant to treatment or show aggressive behavior. Like other tumors, thyroid cancers harbor tumor microenvironment (TME) composed of cancer associated fibroblasts (CAF) and immune cells. Autoimmune lymphocytic thyroiditis can occur in the thyroid, and it may be associated with cancer development. TME is involved in tumor progression through various mechanisms: (1) CAF is involved in tumor progression through cell proliferation and extracellular matrix (ECM) remodeling; and (2) immune cells are involved in tumor progression through cell proliferation, angiogenesis, epithelial mesenchymal transformation (EMT), and immune suppression. These events are activated by various cytokines, chemokines, and metabolites secreted from cells that comprise TME. This review is focused on how CAF and immune cells, two important cell components of thyroid cancer TME, are involved in tumor progression, and will explore their potential as therapeutic targets. Full article
(This article belongs to the Special Issue New Advances in Endocrine-Related Cancer 2022)
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