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Pharmaceuticals
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Targeting Proline Metabolic Pathway for Regulation of Apoptosis/Autophagy in Cancer
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Targeting Proline Metabolic Pathway for Regulation of Apoptosis/Autophagy in Cancer

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

Deadline for manuscript submissions: closed (25 November 2021) | Viewed by 16364

Special Issue Editor

Dr. Wojciech Miltyk

E-Mail Website
Guest Editor
Department of Analysis and Bioanalysis of Medicines, Medical University of Bialystok, Białystok, Poland
Interests: proline metabolism; carcinogenesis; collagen; analysis of medicines

Special Issue Information

Dear Colleagues,

Proline metabolism involves glutamate and ornithine, and enzymatic activity of proline oxidase, ∆1-pyrroline-5-carboxylate (P5C) reductase, P5C dehydrogenase, P5C synthetase, and ornithine d-aminotransferase. The pathway is connected to other essential metabolic cycles: TCA, urea, and pentose phosphate pathway. Disorders in proline metabolism are linked to several diseases. Recent discoveries on the proline metabolism, enzymes involved in proline synthesis and catabolism indicate its important role in tumor growth and cancer progression.

This Special Issue aims to cover the cutting-edge research activities and recent advancements in the area of proline metabolism pathways and factors regulating its activity as a molecular target for cancer treatment.

I cordially invite you to publish your manuscripts in this Pharmaceuticals Special Issue, titled “Targeting Proline Metabolic Pathway for Regulation of Apoptosis/Autophagy in Cancer.”

Dr. Wojciech Miltyk
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

  • Proline
  • Cancer
  • Apoptosis
  • Autophagy
  • Prolidase
  • Proline dehydrogenase/Proline oxidase

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Published Papers (3 papers)

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Research

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13 pages, 1672 KiB  
Article
PRODH/POX-Dependent Celecoxib-Induced Apoptosis in MCF-7 Breast Cancer
by Magdalena Misiura, Ilona Ościłowska, Katarzyna Bielawska, Jerzy Pałka and Wojciech Miltyk
Pharmaceuticals 2021, 14(9), 874; https://doi.org/10.3390/ph14090874 - 29 Aug 2021
Cited by 7 | Viewed by 3198
Abstract
Celecoxib (Cx), an inhibitor of cyclooxygenase 2, induces apoptosis of cancer cells. However, the mechanism of the chemopreventive effect remains not fully understood. We aimed to investigate the role of PRODH/POX that is involved in the regulation of apoptosis induced by celecoxib. MCF-7 [...] Read more.
Celecoxib (Cx), an inhibitor of cyclooxygenase 2, induces apoptosis of cancer cells. However, the mechanism of the chemopreventive effect remains not fully understood. We aimed to investigate the role of PRODH/POX that is involved in the regulation of apoptosis induced by celecoxib. MCF-7 breast cancer cell line and the corresponding MCF-7 cell line with silenced PRODH/POX (MCF-7shPRODH/POX) were used. The effects of Cx on cell viability, proliferation, and cell cycle were evaluated. The expressions of protein markers for apoptosis (Bax, caspase 9, and PARP) and autophagy (Atg5, Beclin 1, and LC3A/B) were investigated by Western immunoblotting. To analyze the proline metabolism, collagen biosynthesis, prolidase activity, proline concentration, and the expression of proline-related proteins were evaluated. The generation of ATP, ROS, and the ratio of NAD+/NADH and NADP+/NADPH were determined to test the effect of Cx on energetic metabolism in breast cancer cells. It has been found that Cx attenuated MCF-7 cell proliferation via arresting the cell cycle. Cx induced apoptosis in MCF-7 breast cancer cells, while in MCF-7shPRODH/POX, autophagy occurred more predominantly. In MCF-7 breast cancer cells, Cx affected proline metabolism through upregulation of proline biosynthesis, PRODH/POX and PYCRs expressions, PEPD activity, and downregulation of collagen biosynthesis. In MCF-7shPRODH/POX clones, these processes, as well as energetic metabolism, were remarkably suppressed. The data for the first time suggest that celecoxib induces apoptosis through upregulation of PRODH/POX in MCF-7 breast cancer cells. Full article
(This article belongs to the Special Issue Targeting Proline Metabolic Pathway for Regulation of Apoptosis/Autophagy in Cancer)
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Review

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27 pages, 1815 KiB  
Review
Free Amino Acid Alterations in Patients with Gynecological and Breast Cancer: A Review
by Dagmara Pietkiewicz, Agnieszka Klupczynska-Gabryszak, Szymon Plewa, Magdalena Misiura, Agnieszka Horala, Wojciech Miltyk, Ewa Nowak-Markwitz, Zenon J. Kokot and Jan Matysiak
Pharmaceuticals 2021, 14(8), 731; https://doi.org/10.3390/ph14080731 - 27 Jul 2021
Cited by 14 | Viewed by 3368
Abstract
Gynecological and breast cancers still remain a significant health problem worldwide. Diagnostic methods are not sensitive and specific enough to detect the disease at an early stage. During carcinogenesis and tumor progression, the cellular need for DNA and protein synthesis increases leading to [...] Read more.
Gynecological and breast cancers still remain a significant health problem worldwide. Diagnostic methods are not sensitive and specific enough to detect the disease at an early stage. During carcinogenesis and tumor progression, the cellular need for DNA and protein synthesis increases leading to changes in the levels of amino acids. An important role of amino acids in many biological pathways, including biosynthesis of proteins, nucleic acids, enzymes, etc., which serve as an energy source and maintain redox balance, has been highlighted in many research articles. The aim of this review is a detailed analysis of the literature on metabolomic studies of gynecology and breast cancers with particular emphasis on alterations in free amino acid profiles. The work includes a brief overview of the metabolomic methodology and types of biological samples used in the studies. Special attention was paid to the possible role of selected amino acids in the carcinogenesis, especially proline and amino acids related to its metabolism. There is a clear need for further research and multiple external validation studies to establish the role of amino acid profiling in diagnosing gynecological and breast cancers. Full article
(This article belongs to the Special Issue Targeting Proline Metabolic Pathway for Regulation of Apoptosis/Autophagy in Cancer)
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20 pages, 1132 KiB  
Review
Targeting the Proline–Glutamine–Asparagine–Arginine Metabolic Axis in Amino Acid Starvation Cancer Therapy
by Macus Tien Kuo, Helen H. W. Chen, Lynn G. Feun and Niramol Savaraj
Pharmaceuticals 2021, 14(1), 72; https://doi.org/10.3390/ph14010072 - 18 Jan 2021
Cited by 31 | Viewed by 8778
Abstract
Proline, glutamine, asparagine, and arginine are conditionally non-essential amino acids that can be produced in our body. However, they are essential for the growth of highly proliferative cells such as cancers. Many cancers express reduced levels of these amino acids and thus require [...] Read more.
Proline, glutamine, asparagine, and arginine are conditionally non-essential amino acids that can be produced in our body. However, they are essential for the growth of highly proliferative cells such as cancers. Many cancers express reduced levels of these amino acids and thus require import from the environment. Meanwhile, the biosynthesis of these amino acids is inter-connected but can be intervened individually through the inhibition of key enzymes of the biosynthesis of these amino acids, resulting in amino acid starvation and cell death. Amino acid starvation strategies have been in various stages of clinical applications. Targeting asparagine using asparaginase has been approved for treating acute lymphoblastic leukemia. Targeting glutamine and arginine starvations are in various stages of clinical trials, and targeting proline starvation is in preclinical development. The most important obstacle of these therapies is drug resistance, which is mostly due to reactivation of the key enzymes involved in biosynthesis of the targeted amino acids and reprogramming of compensatory survival pathways via transcriptional, epigenetic, and post-translational mechanisms. Here, we review the interactive regulatory mechanisms that control cellular levels of these amino acids for amino acid starvation therapy and how drug resistance is evolved underlying treatment failure. Full article
(This article belongs to the Special Issue Targeting Proline Metabolic Pathway for Regulation of Apoptosis/Autophagy in Cancer)
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