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Pharmaceuticals
Special Issues
Pharmacotherapy and Tumor Cell Death
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Pharmacotherapy and Tumor Cell Death

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: closed (27 April 2023) | Viewed by 7476

Special Issue Editor

Prof. Dr. Yongbin Chen

E-Mail Website
Guest Editor
Key Laboratory of Animal Models and Human Disease Mechanisms, Kunming Institute of Zoology, Chinese Academy of Sciences (CAS), Kunming 650201, China
Interests: hypoxic solid tumors; ROS; epigenetic; pharmacotherapy

Special Issue Information

Dear Colleagues,

Cell death is a process of fundamental importance to human health. The induction of cell death forms other than apoptosis has gradually emerged as a new cancer treatment strategy because most tumor cells are resistant to apoptosis. Elucidation of the molecular mechanisms by which tumor cells kill themselves has provided new insights into the origins of malignancy. Cell death induced by pharmacological treatments suppresses tumor proliferation, invasion and metastasis. The pharmacological response of tumor cells is further shaped by various forms of regulated cell death, such as apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence and mitotic catastrophe. However, unrestricted cell death might cause an inflammation-related immunosuppressive microenvironment, leading to tumor progression or recurrence. Therefore, the precise control of tumor cell death induced by different pharmacological treatments should be further studied.

Previous studies have revealed that mutations repressing cell death allow cells to accumulate, prevent the removal of cells with damaged genomes, and increase tumor cell resistance to chemo- and/or radiotherapies. The deciphering of these mechanisms has promoted the development of pharmacological drugs that kill tumor cells by directly activating the cell death machinery to achieve improved outcomes for cancer patients. This Special Issue aims to provide a complete overview of what is already known about the tumor cell death induced by various types of pharmacological treatments, such as natural compounds, small-molecule compounds and Chinese medicines.

Prof. Dr. Yongbin Chen
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. Pharmaceuticals is an international peer-reviewed open access monthly 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

  • pharmacotherapy
  • cancer
  • cell death
  • apoptosis
  • ferroptosis
  • pyroptosis
  • necroptosis
  • alkaliptosis
  • autophagy

Published Papers (4 papers)

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Research

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16 pages, 4244 KiB  
Article
The m6A Reader YTHDF1 Promotes Lung Carcinoma Progression via Regulating Ferritin Mediate Ferroptosis in an m6A-Dependent Manner
by Hongtao Diao, Huiling Tan, Yaju Hu, Ruonan Wang, Pingdong Cai, Bingying Huang, Xiaoqi Shao, Meiling Yan, Chuntong Yin and Yue Zhang
Pharmaceuticals 2023, 16(2), 185; https://doi.org/10.3390/ph16020185 - 25 Jan 2023
Cited by 5 | Viewed by 1433
Abstract
N6-methyladenosine (m6A) plays a significant role as an epigenetic mechanism, which is involved in various cancers’ progress via regulating mRNA modification. As a crucial m6A “reader”, YTHDF1 is able to alter m6A-modified mRNA and promote the protein [...] Read more.
N6-methyladenosine (m6A) plays a significant role as an epigenetic mechanism, which is involved in various cancers’ progress via regulating mRNA modification. As a crucial m6A “reader”, YTHDF1 is able to alter m6A-modified mRNA and promote the protein translation process in multiple cancers. However, the role of YTHDF1 in lung cancer has not been fully investigated. This study focuses on elucidating the function of YTHDF1 in the development of lung cancer and its underlying mechanism. We demonstrated that YTHDF1 was highly expressed in lung carcinoma progression; then, the loss of function experiments in lung cell lines confirmed that knockdown of YTHDF1 suppressed cell proliferation, migration and invasion and induced ferroptosis of lung cancer cells. Further functional assays showed that ferritin (FTH) was identified as the key target of YTHDF1 in lung cancer cells. Furthermore, the overexpression of ferritin in YTHDF1-depleted cells partially restored lung cancer cell suppression. Collectively, our data suggested that the upregulation of YTHDF1 promotes lung cancer carcinogenesis by accelerating ferritin translation in an m6A-dependent manner. We hope that our findings may provide a new target for lung cancer diagnosis and treatment. Full article
(This article belongs to the Special Issue Pharmacotherapy and Tumor Cell Death)
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17 pages, 2635 KiB  
Article
Effects of o,p’-DDE, a Mitotane Metabolite, in an Adrenocortical Carcinoma Cell Line
by Camila Bach, Claudia Rita Corso, Alan de Almeida Veiga, Mariana Martins Paraizo and Lauro Mera de Souza
Pharmaceuticals 2022, 15(12), 1486; https://doi.org/10.3390/ph15121486 - 29 Nov 2022
Cited by 2 | Viewed by 1249
Abstract
In South Brazil, the incidence of pediatric adrenocortical carcinoma (ACC) is higher than in other regions and countries worldwide. The ACC treatment includes therapy with mitotane, the only adrenolytic drug approved by the FDA. The mitotane metabolism occurs via two main reactions: the [...] Read more.
In South Brazil, the incidence of pediatric adrenocortical carcinoma (ACC) is higher than in other regions and countries worldwide. The ACC treatment includes therapy with mitotane, the only adrenolytic drug approved by the FDA. The mitotane metabolism occurs via two main reactions: the β-hydroxylation, which yields the final product o,p’-DDA, and the α-hydroxylation, which will give the final product o,p’-DDE. It is speculated that o,p’-DDE may be an active metabolite since it has a cytotoxic effect on adrenocortical carcinoma cells (H295R). No further studies have been conducted to confirm this hypothesis; however, it was found that mitotane and its metabolites are present at significantly different concentrations in the plasma of the patients. Our study aimed to assess the in vitro effects of o,p’-DDE and o,p’-DDD in cell death pathways, oxidative parameters, and interaction with adrenal CYP’s involved in the steroidogenic process in the H295R cell line. It was found that o,p’-DDE had a different effect than the o,p’-DDD on apoptosis, inhibiting this cell death pathway, but it promotes cell necrosis at higher concentrations. In contrast to o,p’-DDD, the o,p’-DDE did not have effects on the different oxidative parameters evaluated, but exhibited stimulatory interactions with steroidogenic CYP’s, at intermediate concentrations. Therefore, we demonstrated important cell effects of o,p’-DDE; its plasma levels during mitotane therapy should be monitored as an important therapeutic parameter. Full article
(This article belongs to the Special Issue Pharmacotherapy and Tumor Cell Death)
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15 pages, 4253 KiB  
Article
ZLM-7 Blocks Breast Cancer Progression by Inhibiting MDM2 via Upregulation of 14-3-3 Sigma
by Min Wen, Zi-Zheng Zou, Tiao Luo, Xuan Li, Su-You Liu, Ji-Jia Li and Zhi-Yong Luo
Pharmaceuticals 2022, 15(7), 874; https://doi.org/10.3390/ph15070874 - 15 Jul 2022
Cited by 2 | Viewed by 1574
Abstract
Breast cancer is one of the most prevalent malignancies with poor prognosis. Inhibition of angiogenesis is becoming a valid and evident therapeutic strategy to treat cancer. Recent studies uncovered the antiangiogenic activity of ZLM-7 (a combretastain A-4 derivative), but the regulatory mechanism is [...] Read more.
Breast cancer is one of the most prevalent malignancies with poor prognosis. Inhibition of angiogenesis is becoming a valid and evident therapeutic strategy to treat cancer. Recent studies uncovered the antiangiogenic activity of ZLM-7 (a combretastain A-4 derivative), but the regulatory mechanism is unclear. ZLM-7 treatment was applied in estrogen receptor-positive cell MCF-7, triple-negative breast cancer cell MDA-MB-231 and xenograft models. Transfections were conducted to overexpress or knockdown targeted genes. The gene and protein expressions were measured by qPCR and Western blotting assay, respectively. Cell proliferation and apoptosis were evaluated using the CCK8 method, clone formation assay and flow cytometry. We found that ZLM-7 upregulated 14-3-3 sigma expression but downregulated MDM2 expression in breast cancer cells. ZLM-7 delayed cell proliferation, promoted apoptosis and blocked cell-cycle progression in human breast cancer cells in vitro, while those effects were abolished by 14-3-3 sigma knockdown; overexpression of 14-3-3 sigma reproduced the actions of ZLM-7 on the cell cycle, which could be reversed by MDM2 overexpression. In xenograft models, ZLM-7 treatment significantly inhibited tumor growth while the inhibition was attenuated when 14-3-3 sigma was silenced. Collectively, ZLM-7 could inhibit MDM2 via upregulating 14-3-3 sigma expression, thereby blocking the breast cancer progression. Full article
(This article belongs to the Special Issue Pharmacotherapy and Tumor Cell Death)
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Review

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22 pages, 1091 KiB  
Review
Research Progress on Therapeutic Targeting of Cancer-Associated Fibroblasts to Tackle Treatment-Resistant NSCLC
by Chenxin Li, Yusong Qiu and Yong Zhang
Pharmaceuticals 2022, 15(11), 1411; https://doi.org/10.3390/ph15111411 - 15 Nov 2022
Cited by 10 | Viewed by 2535
Abstract
Non-small cell lung cancer (NSCLC) accounts for most lung cancer cases and is the leading cause of cancer-related deaths worldwide. Treatment options for lung cancer are no longer limited to surgery, radiotherapy, and chemotherapy, as targeted therapy and immunotherapy offer a new hope [...] Read more.
Non-small cell lung cancer (NSCLC) accounts for most lung cancer cases and is the leading cause of cancer-related deaths worldwide. Treatment options for lung cancer are no longer limited to surgery, radiotherapy, and chemotherapy, as targeted therapy and immunotherapy offer a new hope for patients. However, drug resistance in chemotherapy and targeted therapy, and the low response rates to immunotherapy remain important challenges. Similar to tumor development, drug resistance occurs because of significant effects exerted by the tumor microenvironment (TME) along with cancer cell mutations. Cancer-associated fibroblasts (CAFs) are a key component of the TME and possess multiple functions, including cross-talking with cancer cells, remodeling of the extracellular matrix (ECM), secretion of various cytokines, and promotion of epithelial-mesenchymal transition, which in turn provide support for the growth, invasion, metastasis, and drug resistance of cancer cells. Therefore, CAFs represent valuable therapeutic targets for lung cancer. Herein, we review the latest progress in the use of CAFs as potential targets and mediators of drug resistance for NSCLC treatment. We explored the role of CAFs on the regulation of the TME and surrounding ECM, with particular emphasis on treatment strategies involving combined CAF targeting within the current framework of cancer treatment. Full article
(This article belongs to the Special Issue Pharmacotherapy and Tumor Cell Death)
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