Cancer Metabolism and Resistance to Cell Death: Novel Therapeutic Perspectives 2nd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 630

Special Issue Editor


E-Mail Website
Guest Editor
Istituto Oncologico Veneto IOV-IRCCS, via Gattamelata 64, 35128 Padova, Italy
Interests: reactive oxygen species; redox homeostasis; electron transport chain; mitochondria; cancer metabolism; apoptosis; anticancer strategies; autophagy; drug development; viruses; angiogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolic rewiring is a common feature of cancer cells which promotes tumorigenesis by sustaining uncontrolled proliferation, survival in an adverse microenvironment, invasion, metastasis and resistance to anticancer therapies. Cancer cells tightly control catabolic and anabolic reactions through a plethora of processes, including oncogenic activation, loss of tumor suppressors, genetic alterations in metabolic genes, epigenetic regulation and modulation by both microRNAs and long non-coding RNAs. Moreover, there is evidence that oncogenic viruses also impinge on these pathways to induce malignant transformation. Evasion of cell death is the leading cause of therapeutic failure. In this regard, cancer metabolism impacts on the response of cancer cells to treatment by activating pro-survival processes, including autophagy, or favoring immune escape by modulating the tumor microenvironment. The pivotal role of metabolic reprogramming in the resistance of cancer cells to different types of cell death, including apoptosis and ferroptosis, provides the rationale for anticancer strategies aimed at rewiring cancer cell metabolism. Such approaches have the potential to enhance the sensitivity of cancer cells to conventional and targeted therapies. This Special Issue of Biomedicines aims at dissecting the multifaceted connections between cancer metabolism and cell death pathways, with a focus on the pharmacological modulation of tumor metabolism as an anticancer strategy.

Dr. Francesco Ciccarese
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. Biomedicines 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 2600 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

  • cancer metabolism
  • cell death
  • oncogenic activation
  • miRNAs and lncRNAs
  • oncogenic viruses
  • sensitization to anticancer therapies

Related Special Issue

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

17 pages, 1512 KiB  
Article
Modulation of Epithelial–Mesenchymal Transition Is a Possible Underlying Mechanism for Inducing Chemoresistance in MIA PaCa-2 Cells against Gemcitabine and Paclitaxel
by Hajime Nakamura, Megumi Watanabe, Kohichi Takada, Tatsuya Sato, Fumihito Hikage, Araya Umetsu, Joji Muramatsu, Masato Furuhashi and Hiroshi Ohguro
Biomedicines 2024, 12(5), 1011; https://doi.org/10.3390/biomedicines12051011 - 3 May 2024
Viewed by 406
Abstract
To elucidate the currently unknown molecular mechanisms responsible for the similarity and difference during the acquirement of resistance against gemcitabine (GEM) and paclitaxel (PTX) in patients with pancreatic carcinoma, we examined two-dimensional (2D) and three-dimensional (3D) cultures of parent MIA PaCa-2 cells (MIA [...] Read more.
To elucidate the currently unknown molecular mechanisms responsible for the similarity and difference during the acquirement of resistance against gemcitabine (GEM) and paclitaxel (PTX) in patients with pancreatic carcinoma, we examined two-dimensional (2D) and three-dimensional (3D) cultures of parent MIA PaCa-2 cells (MIA PaCa-2-PA) and their GEM resistance cell line (MIA PaCa-2-GR) and PTX resistance (MIA PaCa-2-PR). Using these cells, we examined 3D spheroid configurations and cellular metabolism, including mitochondrial and glycolytic functions, with a Seahorse bio-analyzer and RNA sequencing analysis. Compared to the MIA PaCa-2-PA, (1) the formation of the 3D spheroids of MIA PaCa-2-GR or -PR was much slower, and (2) their mitochondrial and glycolytic functions were greatly modulated in MIA PaCa-2-GR or -PR, and such metabolic changes were also different between their 2D and 3D culture conditions. RNA sequencing and bioinformatic analyses of the differentially expressed genes (DEGs) using an ingenuity pathway analysis (IPA) suggested that various modulatory factors related to epithelial –mesenchymal transition (EMT) including STAT3, GLI1, ZNF367, NKX3-2, ZIC2, IFIT2, HEY1 and FBLX, may be the possible upstream regulators and/or causal network master regulators responsible for the acquirement of drug resistance in MIA PaCa-2-GR and -PR. In addition, among the prominently altered DEGs (Log2 fold changes more than 6 or less than −6), FABP5, IQSEC3, and GASK1B were identified as unique genes associated with their antisense RNA or pseudogenes, and among these, FABP5 and GASK1B are known to function as modulators of cancerous EMT. Therefore, the observations reported herein suggest that modulations of cancerous EMT may be key molecular mechanisms that are responsible for inducing chemoresistance against GEM or PTX in MIA PaCa-2 cells. Full article
Back to TopTop