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Cancers
Special Issues
Cell Stress, Metabolism, Tumor Microenvironment in Ovarian Cancer
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Cell Stress, Metabolism, Tumor Microenvironment in Ovarian Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: closed (31 October 2022) | Viewed by 10031

Special Issue Editors

Dr. Cecil Han

E-Mail Website
Guest Editor
Department of Oncology, Georgetown University School of Medicine, Lombardi Comprehensive Cancer Center, Washington, DC, USA
Interests: ovarian cancer; lung cancer; deubiquitination; non-coding RNAs; preclinical models of cancer; novel therapeutics
Dr. Min Soon Cho

E-Mail Website
Guest Editor
Department of Pulmonary Medicine - Research, Division of Internal Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
Interests: ovarian cancer, platelet biology, complement system, immune response, immunotherapy, novel therapeutics; interaction between platelet and complement system; cancer microenvironment

Special Issue Information

Dear Colleagues,

Ovarian cancer is the most lethal malignancy of the female reproductive system. Understanding of ovarian cancer initiation, progression, and metastasis is crucial to overcoming the disease. Genome, transcriptome, and proteome studies have shown that the ovarian tumor microenvironment (TME) plays a vital role in the tumorigenesis and progression of ovarian cancer. Ovarian TME, including malignant cells, contains the extracellular matrix, chemokines, cytokines, integrins, matrix metalloproteinases and other secreted molecules, stromal cells, cancer stem cells, pericytes, cancer-associated fibroblasts, endothelial cells, and immune cells. An advanced understanding of the interaction between ovarian cancer cells and the tumor microenvironment may present novel therapeutic targets for ovarian cancer. This Special Issue is aimed at highlighting recent studies on how various ovarian cancer cell intrinsic stresses, including DNA replication stress, DNA damage, genomic, epigenomic, transcriptomic changes, and metabolic reprograming, impact the tumor microenvironment and ovarian cancer progression and treatment. This issue also discusses the various therapies targeting ovarian cancer and the tumor microenvironment.

Dr. Cecil Han
Dr. Min Soon Cho
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

  • ovarian cancer
  • cell stress
  • tumor microenvironment
  • tumor metabolism
  • metastasis
  • immune response
  • innate immunity
  • adaptive immunity
  • immunotherapy
  • therapeutics

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Published Papers (3 papers)

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Research

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12 pages, 3199 KiB  
Article
CK2-Mediated Phosphorylation Upregulates the Stability of USP13 and Promotes Ovarian Cancer Cell Proliferation
by Juntae Kwon, Jinmin Zhang, Boram Mok and Cecil Han
Cancers 2023, 15(1), 200; https://doi.org/10.3390/cancers15010200 - 29 Dec 2022
Cited by 3 | Viewed by 2002
Abstract
Ubiquitin-specific Peptidase 13 (USP13) is a deubiquitinating enzyme that regulates the stability or function of its substrate. USP13 is highly amplified in human ovarian cancer, and elevated expression of USP13 promotes tumorigenesis and metastasis of ovarian cancer. However, there is little known about [...] Read more.
Ubiquitin-specific Peptidase 13 (USP13) is a deubiquitinating enzyme that regulates the stability or function of its substrate. USP13 is highly amplified in human ovarian cancer, and elevated expression of USP13 promotes tumorigenesis and metastasis of ovarian cancer. However, there is little known about USP13 post-translational modifications and their role in ovarian cancer. Here, we found that USP13 is phosphorylated at Thr122 in ovarian cancer cells. Phosphorylated Thr122 (pT122) on endogenous USP13 was observed in most human ovarian cancer cells, and the abundance of this phosphorylation was correlated to the total level of USP13. We further demonstrated that Casein kinase 2 (CK2) directly interacts with and phosphorylates USP13 at Thr122, which promotes the stability of USP13 protein. Finally, we showed that Threonine 122 is important for cell proliferation of ovarian cancer cells. Our findings may reveal a novel regulatory mechanism for USP13, which may lead to novel therapeutic targeting of USP13 in ovarian cancer. Full article
(This article belongs to the Special Issue Cell Stress, Metabolism, Tumor Microenvironment in Ovarian Cancer)
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14 pages, 2568 KiB  
Article
Platelets Increase the Expression of PD-L1 in Ovarian Cancer
by Min Soon Cho, Hani Lee, Ricardo Gonzalez-Delgado, Dan Li, Tomoyuki Sasano, Wendolyn Carlos-Alcalde, Qing Ma, Jinsong Liu, Anil K. Sood and Vahid Afshar-Kharghan
Cancers 2022, 14(10), 2498; https://doi.org/10.3390/cancers14102498 - 19 May 2022
Cited by 16 | Viewed by 3117
Abstract
The interactions between platelets and cancer cells activate platelets and enhance tumor growth. Platelets increase proliferation and epithelial–mesenchymal transition in cancer cells, inhibit anoikis, enhance the extravasation of cancer cells, and protect circulating tumor cells against natural killer cells. Here, we have identified [...] Read more.
The interactions between platelets and cancer cells activate platelets and enhance tumor growth. Platelets increase proliferation and epithelial–mesenchymal transition in cancer cells, inhibit anoikis, enhance the extravasation of cancer cells, and protect circulating tumor cells against natural killer cells. Here, we have identified another mechanism by which platelets dampen the immune attack on cancer cells. We found that platelets can blunt the antitumor immune response by increasing the expression of inhibitory immune checkpoint (PD-L1) on ovarian cancer cells in vitro and in vivo. Platelets increased PD-L1 in cancer cells via contact-dependent (through NF-κB signaling) and contact-independent (through TFGβR1/Smad signaling) pathways. Inhibition of NF-κB or TGFβR1 signaling in ovarian cancer cells abrogated platelet-induced PD-L1 expression. Reducing platelet counts or inhibiting platelet functions reduced the expression of PD-L1 in ovarian cancer. On the other hand, an increase in platelet counts increased the expression of PD-L1 in tumor-bearing mice. Full article
(This article belongs to the Special Issue Cell Stress, Metabolism, Tumor Microenvironment in Ovarian Cancer)
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Review

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37 pages, 2822 KiB  
Review
Interactions between Platelets and Tumor Microenvironment Components in Ovarian Cancer and Their Implications for Treatment and Clinical Outcomes
by Selin Oncul and Min Soon Cho
Cancers 2023, 15(4), 1282; https://doi.org/10.3390/cancers15041282 - 17 Feb 2023
Cited by 6 | Viewed by 4343
Abstract
Platelets, the primary operatives of hemostasis that contribute to blood coagulation and wound healing after blood vessel injury, are also involved in pathological conditions, including cancer. Malignancy-associated thrombosis is common in ovarian cancer patients and is associated with poor clinical outcomes. Platelets extravasate [...] Read more.
Platelets, the primary operatives of hemostasis that contribute to blood coagulation and wound healing after blood vessel injury, are also involved in pathological conditions, including cancer. Malignancy-associated thrombosis is common in ovarian cancer patients and is associated with poor clinical outcomes. Platelets extravasate into the tumor microenvironment in ovarian cancer and interact with cancer cells and non-cancerous elements. Ovarian cancer cells also activate platelets. The communication between activated platelets, cancer cells, and the tumor microenvironment is via various platelet membrane proteins or mediators released through degranulation or the secretion of microvesicles from platelets. These interactions trigger signaling cascades in tumors that promote ovarian cancer progression, metastasis, and neoangiogenesis. This review discusses how interactions between platelets, cancer cells, cancer stem cells, stromal cells, and the extracellular matrix in the tumor microenvironment influence ovarian cancer progression. It also presents novel potential therapeutic approaches toward this gynecological cancer. Full article
(This article belongs to the Special Issue Cell Stress, Metabolism, Tumor Microenvironment in Ovarian Cancer)
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