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Cells
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Cellular and Molecular Mechanisms in Gynecological Disorders
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Cellular and Molecular Mechanisms in Gynecological Disorders

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Reproductive Cells and Development".

Deadline for manuscript submissions: 30 December 2024 | Viewed by 5151

Special Issue Editor

Dr. Qiwei Yang

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Guest Editor
Department of Obstetrics and Gynecology, University of Chicago, Chicago, IL 60637, USA
Interests: reproductive medicine, gynecology; cancer biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Gynecological disorders refer to health issues in the female reproductive organs, including the  uterus, ovaries, fallopian tubes, cervix, vagina, and external genitalia. Gynecological diseases affect women’s life with significant morbidity and represent significant societal health and financial burdens. The associated etiologies are complex and generally not fully understood and our knowledge about the risk factors causing various gynecological disorders is limited. Therefore, better characterization and understanding of the cellular and molecular events driving gynecological diseases are critical to preventing and treating these women’s diseases. 

This Special Issue aims to provide an overview of the current developments and outline future prospectives in gynecological disorders, including ovary-related diseases (polycystic ovary syndrome, ovarian cysts, primary ovarian insufficiency, ovarian cancer), uterine diseases (endometriosis, uterine fibroids, adenomyosis, uterine cancers, such as endometrial cancer, leiomyosarcoma), breast cancer, as well as cervical and vaginal diseases, among others. We welcome submissions of original research, review articles, and short communication related to understanding the key molecules, biological pathways, genome, epigenome, and cell atlas in gynecological disorders. Submissions of topics in the field of basic and translational research are welcome.

Dr. Qiwei Yang
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. 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

  • uterus
  • ovary
  • breast
  • cervix
  • cancer
  • endometriosis
  • leiomyoma
  • adenomyosis
  • polycystic ovary syndrome
  • female infertility
  • pathways
  • cell atlas
  • transcriptome
  • epigenome

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Published Papers (3 papers)

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Research

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20 pages, 8325 KiB  
Article
Unraveling the Role of Bromodomain and Extra-Terminal Proteins in Human Uterine Leiomyosarcoma
by Qiwei Yang, Ali Falahati, Azad Khosh, Ricardo R. Lastra, Thomas G. Boyer and Ayman Al-Hendy
Cells 2024, 13(17), 1443; https://doi.org/10.3390/cells13171443 - 28 Aug 2024
Viewed by 1129
Abstract
Uterine leiomyosarcoma (uLMS) is the most common type of uterine sarcoma, associated with poor prognosis, high rates of recurrence, and metastasis. Currently, the molecular mechanism of the origin and development of uLMS is limited. Bromodomain and extra-terminal (BET) proteins are involved in both [...] Read more.
Uterine leiomyosarcoma (uLMS) is the most common type of uterine sarcoma, associated with poor prognosis, high rates of recurrence, and metastasis. Currently, the molecular mechanism of the origin and development of uLMS is limited. Bromodomain and extra-terminal (BET) proteins are involved in both physiological and pathological events. However, the role of BET proteins in the pathogenesis of uLMS is unknown. Here, we show for the first time that BET protein family members, BRD2, BRD3, and BRD4, are aberrantly overexpressed in uLMS tissues compared to the myometrium, with a significant change by histochemical scoring assessment. Furthermore, inhibiting BET proteins with their small, potent inhibitors (JQ1 and I-BET 762) significantly inhibited the uLMS proliferation dose-dependently via cell cycle arrest. Notably, RNA-sequencing analysis revealed that the inhibition of BET proteins with JQ1 and I-BET 762 altered several critical pathways, including the hedgehog pathway, EMT, and transcription factor-driven pathways in uLMS. In addition, the targeted inhibition of BET proteins altered several other epigenetic regulators, including DNA methylases, histone modification, and m6A regulators. The connections between BET proteins and crucial biological pathways provide a fundamental structure to better understand uterine diseases, particularly uLMS pathogenesis. Accordingly, targeting the vulnerable epigenome may provide an additional regulatory mechanism for uterine cancer treatment. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Gynecological Disorders)
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12 pages, 4440 KiB  
Article
Somatic MED12 Mutations in Myometrial Cells
by Yinuo Li, Huma Asif, Yue Feng, Julie J. Kim and Jian-Jun Wei
Cells 2024, 13(17), 1432; https://doi.org/10.3390/cells13171432 - 27 Aug 2024
Viewed by 690
Abstract
Over 70% of leiomyoma (LM) harbor MED12 mutations, primarily in exon 2 at c.130-131 (GG). Myometrial cells are the cell origin of leiomyoma, but the MED12 mutation status in non-neoplastic myometrial cells is unknown. In this study, we investigated the mutation burden of [...] Read more.
Over 70% of leiomyoma (LM) harbor MED12 mutations, primarily in exon 2 at c.130-131 (GG). Myometrial cells are the cell origin of leiomyoma, but the MED12 mutation status in non-neoplastic myometrial cells is unknown. In this study, we investigated the mutation burden of MED12 in myometrium. As traditional Sanger or even NGS sequencing may not be able to detect MED12 mutations that are lower than 0.1% in the testing sample, we used duplex deep sequencing analysis (DDS) to overcome this limitation. Tumor-free myometria (confirmed by pathology evaluation) were dissected, and genomic DNA from MED12 exon 2 (test) and TP53 exon 5 (control) were captured by customer-designed probe sets, followed by DDS. Notably, DDS demonstrated that myometrial cells harbored a high frequency of mutations in MED12 exon 2 and predominantly in code c.130-131. In contrast, the baseline mutations in other coding sequences of MED12 exon 2 as well as in the TP53 mutation hotspot, c.477-488 were comparably low in myometrial cells. This is the first report demonstrating a non-random accumulation of MED12 mutations at c.130-131 sites in non-neoplastic myometrial cells which provide molecular evidence of early somatic mutation events in myometrial cells. This early mutation may contribute to the cell origin for uterine LM development in women of reproductive age. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Gynecological Disorders)
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Review

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21 pages, 3455 KiB  
Review
Autophagy and Female Fertility: Mechanisms, Clinical Implications, and Emerging Therapies
by Abdel Halim Harrath, Md Ataur Rahman, Sujay Kumar Bhajan, Anup Kumar Bishwas, MD. Hasanur Rahman, Saleh Alwasel, Maroua Jalouli, Sojin Kang, Moon Nyeo Park and Bonglee Kim
Cells 2024, 13(16), 1354; https://doi.org/10.3390/cells13161354 - 14 Aug 2024
Viewed by 2590
Abstract
Autophagy, an evolutionarily conserved cellular mechanism essential for maintaining internal stability, plays a crucial function in female reproductive ability. In this review, we discuss the complex interplay between autophagy and several facets of female reproductive health, encompassing pregnancy, ovarian functions, gynecologic malignancies, endometriosis, [...] Read more.
Autophagy, an evolutionarily conserved cellular mechanism essential for maintaining internal stability, plays a crucial function in female reproductive ability. In this review, we discuss the complex interplay between autophagy and several facets of female reproductive health, encompassing pregnancy, ovarian functions, gynecologic malignancies, endometriosis, and infertility. Existing research emphasizes the crucial significance of autophagy in embryo implantation, specifically in the endometrium, highlighting its necessity in ensuring proper fetal development. Although some knowledge has been gained, there is still a lack of research on the specific molecular impacts of autophagy on the quality of oocytes, the growth of follicles, and general reproductive health. Autophagy plays a role in the maturation, quality, and development of oocytes. It is also involved in reproductive aging, contributing to reductions in reproductive function that occur with age. This review explores the physiological functions of autophagy in the female reproductive system, its participation in reproductive toxicity, and its important connections with the endometrium and embryo. In addition, this study investigates the possibility of emerging treatment approaches that aim to modify autophagy, using both natural substances and synthetic molecules, to improve female fertility and reproductive outcomes. Additionally, this review intends to inspire future exploration into the intricate role of autophagy in female reproductive health by reviewing recent studies and pinpointing areas where current knowledge is lacking. Subsequent investigations should prioritize the conversion of these discoveries into practical uses in the medical field, which could potentially result in groundbreaking therapies for infertility and other difficulties related to reproduction. Therefore, gaining a comprehensive understanding of the many effects of autophagy on female fertility would not only further the field of reproductive biology but also open new possibilities for diagnostic and treatment methods. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Gynecological Disorders)
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