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Molecular Insight into Ovarian Cancer
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Molecular Insight into Ovarian Cancer

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

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 5915

Special Issue Editors

Dr. Karen Kar Loen Chan

E-Mail Website
Guest Editor
Department of Obstetrics & Gynaecology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China
Interests: gynaecological oncology; general gynaecology; hormonal treatment; tumor microenvironment; tumor glycolysis and human papillomavirus
Dr. David Wai Chan

E-Mail Website
Guest Editor
School of Medicine, The Chinese University of Hong Kong-Shenzhen, Shenzhen, China
Interests: tumor–stroma interactions; circulating biomarkers; miRNAs; tumor microenvironment; cancer cell metabolism; macrophage polarization; ovarian cancer; tumor evolution; animal models; organoids; combined treatment

Special Issue Information

Dear Colleagues,

Epithelial ovarian cancer (EOC) is one of the most lethal malignancies affecting women worldwide. The high mortality rate of this disease is due to the lack of a reliable screening strategy, which results in the majority of cases of this disease being diagnosed at an advanced stage associated with a poor prognosis due to increased chemoresistance, extensive metastasis, and high recurrence.  Hence, the exploration of reliable biomarkers or methods in tumor screening and the development of novel and innovative therapeutic strategies to overcome chemoresistance and inhibit cancer metastasis are the central goals in ovarian cancer research. The recent advancement in omics technology has provided crucial insight into the genetic and epigenetic heterogeneity of ovarian cancer development and progression. This Special Issue aims to collate the latest research regarding the following topics:

  1. The novel biomarkers and trends in ovarian cancer screening.
  2. The role of epigenetic and genetic alterations in ovarian cancers.
  3. The metabolic impacts on tumor development and progression.
  4. Novel strategies or tools for monitoring tumor growth and metastasis.
  5. The new and efficient models for studying ovarian cancer chemoresistance and metastasis.
  6. New or potential treatment options for ovarian cancers.

Dr. Karen Kar Loen Chan
Dr. David Wai Chan
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 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

  • ovarian cancers
  • metastatic progression
  • tumor–stroma interactions
  • tumor microenvironment
  • onco-immunology
  • chemoresistance
  • cancer cell metabolism
  • circulating miRNAs
  • organoid culture
  • drug synergism
  • miRNAs

Published Papers (3 papers)

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Research

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41 pages, 12661 KiB  
Article
Increased Expression of the RBPMS Splice Variants Inhibits Cell Proliferation in Ovarian Cancer Cells
by Robert J. Rabelo-Fernández, Ricardo A. Noriega Rivera, Yasmarie Santana Rivera, José Tous-Beveraggi, Fatima Valiyeva and Pablo E. Vivas-Mejia
Int. J. Mol. Sci. 2022, 23(23), 14742; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232314742 - 25 Nov 2022
Cited by 4 | Viewed by 1799
Abstract
RNA-Binding Protein with Multiple Splicing (RBPMS) is a member of family proteins that bind to nascent RNA transcripts and regulate their splicing, localization, and stability. Evidence indicates that RBPMS controls the activity of transcription factors associated with cell growth and proliferation, including AP-1 [...] Read more.
RNA-Binding Protein with Multiple Splicing (RBPMS) is a member of family proteins that bind to nascent RNA transcripts and regulate their splicing, localization, and stability. Evidence indicates that RBPMS controls the activity of transcription factors associated with cell growth and proliferation, including AP-1 and Smads. Three major RBPMS protein splice variants (RBPMSA, RBPMSB, and RBPMSC) have been described in the literature. We previously reported that reduced RBPMS levels decreased the sensitivity of ovarian cancer cells to cisplatin treatment. However, little is known about the biological role of the RBPMS splice variants in ovarian cancer cells. We performed RT-PCR and Western blots and observed that both RBPMSA and RBPMSC are reduced at the mRNA and protein levels in cisplatin resistant as compared with cisplatin sensitive ovarian cancer cells. The mRNA and protein levels of RBPMSB were not detectable in any of the ovarian cancer cells tested. To better understand the biological role of each RBPMSA and RBPMSC, we transfected these two splice variants in the A2780CP20 and OVCAR3CIS cisplatin resistant ovarian cancer cells and performed cell proliferation, cell migration, and invasion assays. Compared with control clones, a significant reduction in the number of colonies, colony size, cell migration, and invasion was observed with RBPMSA and RBPMSC overexpressed cells. Moreover, A2780CP20-RBPMSA and A2780CP20-RBPMSC clones showed reduced senescence-associated β-galactosidase (β-Gal)-levels when compared with control clones. A2780CP20-RBPMSA clones were more sensitive to cisplatin treatment as compared with A2780CP20-RBPMSC clones. The A2780CP20-RBPMSA and A2780CP20-RBPMSC clones subcutaneously injected into athymic nude mice formed smaller tumors as compared with A2780CP20-EV control group. Additionally, immunohistochemical analysis showed lower proliferation (Ki67) and angiogenesis (CD31) staining in tissue sections of A2780CP20-RBPMSA and A2780CP20-RBPMSC tumors compared with controls. RNAseq studies revealed many common RNA transcripts altered in A2780CP20-RBPMSA and A2780CP20-RBPMSC clones. Unique RNA transcripts deregulated by each RBPMS variant were also observed. Kaplan–Meier (KM) plotter database information identified clinically relevant RBPMSA and RBPMSC downstream effectors. These studies suggest that increased levels of RBPMSA and RBPMSC reduce cell proliferation in ovarian cancer cells. However, only RBPMSA expression levels were associated with the sensitivity of ovarian cancer cells to cisplatin treatment. Full article
(This article belongs to the Special Issue Molecular Insight into Ovarian Cancer)
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Review

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17 pages, 1151 KiB  
Review
New Insights into Ferroptosis Initiating Therapies (FIT) by Targeting the Rewired Lipid Metabolism in Ovarian Cancer Peritoneal Metastases
by Shijie Zhan, Mingo M. H. Yung, Michelle K. Y. Siu, Peili Jiao, Hextan Y. S. Ngan, David W. Chan and Karen K. L. Chan
Int. J. Mol. Sci. 2022, 23(23), 15263; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232315263 - 03 Dec 2022
Cited by 6 | Viewed by 2262
Abstract
Ovarian cancer is one of the most lethal gynecological cancers worldwide. The poor prognosis of this malignancy is substantially attributed to the inadequate symptomatic biomarkers for early diagnosis and effective remedies to cure the disease against chemoresistance and metastasis. Ovarian cancer metastasis is [...] Read more.
Ovarian cancer is one of the most lethal gynecological cancers worldwide. The poor prognosis of this malignancy is substantially attributed to the inadequate symptomatic biomarkers for early diagnosis and effective remedies to cure the disease against chemoresistance and metastasis. Ovarian cancer metastasis is often relatively passive, and the single clusters of ovarian cancer cells detached from the primary ovarian tumor are transcoelomic spread by the peritoneal fluid throughout the peritoneum cavity and omentum. Our earlier studies revealed that lipid-enriched ascitic/omental microenvironment enforced metastatic ovarian cancer cells to undertake metabolic reprogramming and utilize free fatty acids as the main energy source for tumor progression and aggression. Intriguingly, cell susceptibility to ferroptosis has been tightly correlated with the dysregulated fatty acid metabolism (FAM), and enhanced iron uptake as the prominent features of ferroptosis are attributed to the strengthened lipid peroxidation and aberrant iron accumulation, suggesting that ferroptosis induction is a targetable vulnerability to prevent cancer metastasis. Therefore, the standpoints about tackling altered FAM in combination with ferroptosis initiation as a dual-targeted therapy against advanced ovarian cancer were highlighted herein. Furthermore, a discussion on the prospect and challenge of inducing ferroptosis as an innovative therapeutic approach for reversing remedial resistance in cancer interventions was included. It is hoped this proof-of-concept review will indicate appropriate directions for speeding up the translational application of ferroptosis-inducing compounds (FINs) to improve the efficacy of ovarian cancer treatment. Full article
(This article belongs to the Special Issue Molecular Insight into Ovarian Cancer)
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20 pages, 898 KiB  
Review
E-Cadherin Expression in Relation to Clinicopathological Parameters and Survival of Patients with Epithelial Ovarian Cancer
by Michal Kielbik, Izabela Szulc-Kielbik and Magdalena Klink
Int. J. Mol. Sci. 2022, 23(22), 14383; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232214383 - 19 Nov 2022
Cited by 5 | Viewed by 1335
Abstract
It is generally accepted that loss/reduction of E-cadherin expression on tumor cells promotes their migration, invasiveness, and metastasis. It is also an indicator of cancer cells’ aggressiveness. The aim of this study was to assess how the expression of E-cadherin varies in primary [...] Read more.
It is generally accepted that loss/reduction of E-cadherin expression on tumor cells promotes their migration, invasiveness, and metastasis. It is also an indicator of cancer cells’ aggressiveness. The aim of this study was to assess how the expression of E-cadherin varies in primary ovarian cancer tissue in regard to overall survival of patients; FIGO stage; grade; histopathological type of tumor; and potential factors discriminating malignant and nonmalignant ovarian tumors. Our analysis was based on literature research (1 January 2000–8 November 2021) conducted according to the PRISMA guidelines. Most studies support the assumption that loss/reduced expression of E-cadherin results in shorter overall survival of EOC patients. Moreover, most research has shown that there is a correlation between the low level of E-cadherin and the advancement stage of disease, especially in high-grade serous ovarian carcinoma type. However, E-cadherin expression seems to not be helpful to distinguish malignant and nonmalignant tumors. In conclusion, reduced E-cadherin expression in primary ovarian cancer tissue may indicate a less favorable disease outcome and is associated with high advancement of the disease. Full article
(This article belongs to the Special Issue Molecular Insight into Ovarian Cancer)
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