Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
7.4
5.2
Journals
Cancers
Special Issues
The Biological Mechanism of Cancer Proliferation and Metastasis
share announcement

The Biological Mechanism of Cancer Proliferation and Metastasis

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (15 April 2023) | Viewed by 14557

Special Issue Editor

Dr. Abhishek Tyagi

E-Mail Website
Guest Editor
Department of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA
Interests: tumor metastasis; tumor immunology; tumor metabolism; tumor virology (HPV); radio-resistance; immunotherapy resistance
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Cancer is a genetic disease by definition, and it has traditionally been studied from this perspective. Although we still lack a complete understanding of the specific complement that together program the behavior of any particular cancer, several lines of evidence indicate that many of these alterations perturb regulatory networks critical for cell proliferation, growth, and survival. As a result, cancer cells strike a delicate balance between unrestricted proliferation, genomic instability, cell cycle arrest, and apoptosis. The surrounding tumor microenvironment, on the other hand, is critical for keeping cancer cells alive and for determining tumor progression and response to therapy. Despite advancements in cancer diagnosis and treatment, cancer metastasis remains an unsolved problem. Around 90% of cancer patients die as a result of metastatic disease. Yet, the cellular and molecular mechanisms driving the formation of these secondary tumors remain only partially solved. The current challenge is to improve our understanding of metastasis and identify machineries that are ideal targets for anti-metastatic strategies that could help in the improvement of therapy results and clinical outcome in cancer patients.

The Cancers journal publishes research that is both fundamental and translational. Original reviews, research articles, mini-reviews, and technical (methodology) papers that discuss therapeutic options based on specific molecular features of primary and secondary (metastatic) tumors are invited for its Special Issue “The Biological Mechanism of Cancer Proliferation and Metastasis”. In particular, we invite articles that expose novel mechanisms of solid cancer progression and metastasis, with an eye on novel therapeutic targeting. We welcome manuscripts that use clinical data and preclinical animal models to describe/discuss oncogenic processes that promote tumor invasion, dissemination, dormancy, the role of the microenvironment (tumor stroma and immune system) in metastatic progression, tumor metabolism, and therapy resistance mechanism (radio-, chemo-, immune-) in the primary, invasive front, and metastatic niches.

We look forward to receiving your contributions.

Dr. Abhishek Tyagi
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. 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

  • solid cancer
  • invasion
  • progression
  • metastasis
  • tumor immune microenvironment
  • stemness EMT
  • MET
  • dormancy
  • metabolic profiling
  • therapy resistance

Published Papers (8 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Editorial

Jump to: Research, Review

2 pages, 184 KiB  
Editorial
Underlying Facets of Cancer Metastasis
by Abhishek Tyagi
Cancers 2022, 14(12), 2989; https://doi.org/10.3390/cancers14122989 - 17 Jun 2022
Cited by 1 | Viewed by 1265
Abstract
Even though metastasis, a hallmark of cancer, is responsible for up to 90% of cancer-related mortality, it is still the least understood aspect of cancer pathogenesis [...] Full article
(This article belongs to the Special Issue The Biological Mechanism of Cancer Proliferation and Metastasis)

Research

Jump to: Editorial, Review

15 pages, 3778 KiB  
Article
The β-Secretase 1 Enzyme as a Novel Therapeutic Target for Prostate Cancer
by Hilal A. Rather, Sameh Almousa, Ashish Kumar, Mitu Sharma, Isabel Pennington, Susy Kim, Yixin Su, Yangen He, Abdollah R. Ghara, Kiran Kumar Solingapuram Sai, Nora M. Navone, Donald J. Vander Griend and Gagan Deep
Cancers 2024, 16(1), 10; https://doi.org/10.3390/cancers16010010 - 19 Dec 2023
Viewed by 986
Abstract
Recent studies have demonstrated the association of APP and Aβ with cancer, suggesting that BACE1 may play an important role in carcinogenesis. In the present study, we assessed BACE1’s usefulness as a therapeutic target in prostate cancer (PCa). BACE1 expression was observed in [...] Read more.
Recent studies have demonstrated the association of APP and Aβ with cancer, suggesting that BACE1 may play an important role in carcinogenesis. In the present study, we assessed BACE1’s usefulness as a therapeutic target in prostate cancer (PCa). BACE1 expression was observed in human PCa tissue samples, patient-derived xenografts (PDX), human PCa xenograft tissue in nude mice, and transgenic adenocarcinoma of the mouse prostate (TRAMP) tissues by immunohistochemistry (IHC) analysis. Additionally, the downstream product of BACE1 activity, i.e., Aβ1-42 expression, was also observed in these PCa tissues by IHC as well as by PET imaging in TRAMP mice. Furthermore, BACE1 gene expression and activity was confirmed in several established PCa cell lines (LNCaP, C4-2B-enzalutamide sensitive [S], C4-2B-enzalutamide resistant [R], 22Rv1-S, 22Rv1-R, PC3, DU145, and TRAMP-C1) by real-time PCR and fluorometric assay, respectively. Treatment with a pharmacological inhibitor of BACE1 (MK-8931) strongly reduced the proliferation of PCa cells in in vitro and in vivo models, analyzed by multiple assays (MTT, clonogenic, and trypan blue exclusion assays and IHC). Cell cycle analyses revealed an increase in the sub-G1 population and a significant modulation in other cell cycle stages (G1/S/G2/M) following MK-8931 treatment. Most importantly, in vivo administration of MK-8931 intraperitoneal (30 mg/kg) strongly inhibited TRAMP-C1 allograft growth in immunocompetent C57BL/6 mice (approximately 81% decrease, p = 0.019). Furthermore, analysis of tumor tissue using the prostate cancer-specific pathway array revealed the alteration of several genes involved in PCa growth and progression including Forkhead O1 (FOXO1). All together, these findings suggest BACE1 as a novel therapeutic target in advanced PCa. Full article
(This article belongs to the Special Issue The Biological Mechanism of Cancer Proliferation and Metastasis)
►▼ Show Figures

Figure 1

17 pages, 2064 KiB  
Article
Genetic Ablation of the MET Oncogene Defines a Crucial Role of the HGF/MET Axis in Cell-Autonomous Functions Driving Tumor Dissemination
by Chiara Modica, Marco Cortese, Francesca Bersani, Andrea Maria Lombardi, Francesca Napoli, Luisella Righi, Riccardo Taulli, Cristina Basilico and Elisa Vigna
Cancers 2023, 15(10), 2742; https://doi.org/10.3390/cancers15102742 - 13 May 2023
Viewed by 1192
Abstract
Cancer cell dissemination is sustained by cell-autonomous and non-cell-autonomous functions. To disentangle the role of HGF (Hepatocyte Growth Factor) and MET ligand/receptor axis in this complex process, we genetically knocked out the MET gene in cancer cells in which MET is not the [...] Read more.
Cancer cell dissemination is sustained by cell-autonomous and non-cell-autonomous functions. To disentangle the role of HGF (Hepatocyte Growth Factor) and MET ligand/receptor axis in this complex process, we genetically knocked out the MET gene in cancer cells in which MET is not the oncogenic driver. In this way, we evaluated the contribution of the HGF/MET axis to cancer cell dissemination independently of its direct activities in cells of the tumor microenvironment. The lack of MET expression in MET−/− cells has been proved by molecular characterization. From a functional point of view, HGF stimulation of MET−/− cancer cells was ineffective in eliciting intracellular signaling and in sustaining biological functions predictive of malignancy in vitro (i.e., anchorage-independent growth, invasion, and survival in the absence of matrix adhesion). Cancer cell dissemination was assessed in vivo, evaluating: (i) the ability of MET−/− lung carcinoma cells to colonize the lungs following intravenous injection and (ii) the spontaneous dissemination to distant organs of MET−/− pancreatic carcinoma cells upon orthotopic injection. In both experimental models, MET ablation affects the time of onset, the number, and the size of metastatic lesions. These results define a crucial contribution of the HGF/MET axis to cell-autonomous functions driving the metastatic process. Full article
(This article belongs to the Special Issue The Biological Mechanism of Cancer Proliferation and Metastasis)
►▼ Show Figures

Figure 1

17 pages, 7328 KiB  
Article
c-Met Mediated Cytokine Network Promotes Brain Metastasis of Breast Cancer by Remodeling Neutrophil Activities
by Yin Liu, Margaret R. Smith, Yuezhu Wang, Ralph D’Agostino, Jr., Jimmy Ruiz, Thomas Lycan, Gregory L. Kucera, Lance D. Miller, Wencheng Li, Michael D. Chan, Michael Farris, Jing Su, Qianqian Song, Dawen Zhao, Arvind Chandrasekaran and Fei Xing
Cancers 2023, 15(9), 2626; https://doi.org/10.3390/cancers15092626 - 5 May 2023
Cited by 3 | Viewed by 2172
Abstract
The brain is one of the most common metastatic sites among breast cancer patients, especially in those who have Her2-positive or triple-negative tumors. The brain microenvironment has been considered immune privileged, and the exact mechanisms of how immune cells in the brain microenvironment [...] Read more.
The brain is one of the most common metastatic sites among breast cancer patients, especially in those who have Her2-positive or triple-negative tumors. The brain microenvironment has been considered immune privileged, and the exact mechanisms of how immune cells in the brain microenvironment contribute to brain metastasis remain elusive. In this study, we found that neutrophils are recruited and influenced by c-Met high brain metastatic cells in the metastatic sites, and depletion of neutrophils significantly suppressed brain metastasis in animal models. Overexpression of c-Met in tumor cells enhances the secretion of a group of cytokines, including CXCL1/2, G-CSF, and GM-CSF, which play critical roles in neutrophil attraction, granulopoiesis, and homeostasis. Meanwhile, our transcriptomic analysis demonstrated that conditioned media from c-Met high cells significantly induced the secretion of lipocalin 2 (LCN2) from neutrophils, which in turn promotes the self-renewal of cancer stem cells. Our study unveiled the molecular and pathogenic mechanisms of how crosstalk between innate immune cells and tumor cells facilitates tumor progression in the brain, which provides novel therapeutic targets for treating brain metastasis. Full article
(This article belongs to the Special Issue The Biological Mechanism of Cancer Proliferation and Metastasis)
►▼ Show Figures

Figure 1

20 pages, 6145 KiB  
Article
PGC-1α Regulates Cell Proliferation, Migration, and Invasion by Modulating Leucyl-tRNA Synthetase 1 Expression in Human Colorectal Cancer Cells
by Jun Gi Cho, Su-Jeong Park, Sang-Heum Han and Joo-In Park
Cancers 2023, 15(1), 159; https://doi.org/10.3390/cancers15010159 - 27 Dec 2022
Cited by 3 | Viewed by 1671
Abstract
Although mounting evidence has demonstrated that peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) can promote tumorigenesis, its role in cancer remains controversial. To find potential target molecules of PGC-1α, GeneFishingTM DEG (differentially expressed genes) screening was performed using stable HEK293 cell lines [...] Read more.
Although mounting evidence has demonstrated that peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) can promote tumorigenesis, its role in cancer remains controversial. To find potential target molecules of PGC-1α, GeneFishingTM DEG (differentially expressed genes) screening was performed using stable HEK293 cell lines expressing PGC-1α (PGC-1α-HEK293). As results, leucyl-tRNA synthetase 1 (LARS1) was upregulated. Western blot analysis showed that LARS1 was increased in PGC-1α overexpressed SW480 cells but decreased in PGC-1α shRNA knockdown SW620 cells. Several studies have suggested that LARS1 can be a potential target of anticancer agents. However, the molecular network of PGC-1α and LARS1 in human colorectal cancer cells remains unclear. LARS1 overexpression enhanced cell proliferation, migration, and invasion, whereas LARS1 knockdown reduced them. We also observed that expression levels of cyclin D1, c-Myc, and vimentin were regulated by LARS1 expression. We aimed to investigate whether effects of PGC-1α on cell proliferation and invasion were mediated by LARS1. Our results showed that PGC-1α might modulate cell proliferation and invasion by regulating LARS1 expression. These results suggest that LARS1 inhibitors might be used as anticancer agents in PGC-1α-overexpressing colorectal cancer. Further studies are needed in the future to clarify the detailed molecular mechanism by which PGC-1α regulates LARS1 expression. Full article
(This article belongs to the Special Issue The Biological Mechanism of Cancer Proliferation and Metastasis)
►▼ Show Figures

Figure 1

Review

Jump to: Editorial, Research

16 pages, 1012 KiB  
Review
Plexins as Regulators of Cancer Cell Proliferation, Migration, and Invasivity
by Shira Toledano and Gera Neufeld
Cancers 2023, 15(16), 4046; https://doi.org/10.3390/cancers15164046 - 10 Aug 2023
Cited by 2 | Viewed by 1338
Abstract
Plexins are a family of nine single-pass transmembrane receptors with a conserved GTPase activating protein (GAP) domain. The plexin family is divided into four subfamilies: Type-A, type-B, type-C, and type-D plexins. Plexins function as receptors for axon guidance factors of the semaphorin family. [...] Read more.
Plexins are a family of nine single-pass transmembrane receptors with a conserved GTPase activating protein (GAP) domain. The plexin family is divided into four subfamilies: Type-A, type-B, type-C, and type-D plexins. Plexins function as receptors for axon guidance factors of the semaphorin family. The semaphorin gene family contains 22 genes that are divided into eight subclasses of which subclasses three to seven represent vertebrate semaphorins. The plexins and their semaphorin ligands have important roles as regulators of angiogenesis, cancer proliferation, and metastasis. Class 3 semaphorins, with the exception of sema3E, are the only semaphorins that do not bind directly to plexins. In order to transduce their signals, they bind instead to complexes consisting of receptors of the neuropilin family and various plexins. Some plexins also form complexes with tyrosine-kinase receptors such as the epidermal growth factor receptor ErbB2, the mesenchymal epithelial transition factor receptor (MET), and the Vascular endothelial growth factor receptor 2 (VEGFR2) and, as a result, can modulate cell proliferation and tumor progression. This review focuses on the roles of the different plexins in the control of cancer cell proliferation and invasiveness. Plexins also affect tumor progression and tumor metastasis by indirect mechanisms, such as modulation of angiogenesis and immune responses. However, these topics are not covered in the present review. Full article
(This article belongs to the Special Issue The Biological Mechanism of Cancer Proliferation and Metastasis)
►▼ Show Figures

Figure 1

27 pages, 1488 KiB  
Review
Surface-Engineered Extracellular Vesicles in Cancer Immunotherapy
by Vinith Johnson, Sunil Vasu, Uday S. Kumar and Manoj Kumar
Cancers 2023, 15(10), 2838; https://doi.org/10.3390/cancers15102838 - 19 May 2023
Cited by 8 | Viewed by 2720
Abstract
Extracellular vesicles (EVs) are lipid bilayer-enclosed bodies secreted by all cell types. EVs carry bioactive materials, such as proteins, lipids, metabolites, and nucleic acids, to communicate and elicit functional alterations and phenotypic changes in the counterpart stromal cells. In cancer, cells secrete EVs [...] Read more.
Extracellular vesicles (EVs) are lipid bilayer-enclosed bodies secreted by all cell types. EVs carry bioactive materials, such as proteins, lipids, metabolites, and nucleic acids, to communicate and elicit functional alterations and phenotypic changes in the counterpart stromal cells. In cancer, cells secrete EVs to shape a tumor-promoting niche. Tumor-secreted EVs mediate communications with immune cells that determine the fate of anti-tumor therapeutic effectiveness. Surface engineering of EVs has emerged as a promising tool for the modulation of tumor microenvironments for cancer immunotherapy. Modification of EVs’ surface with various molecules, such as antibodies, peptides, and proteins, can enhance their targeting specificity, immunogenicity, biodistribution, and pharmacokinetics. The diverse approaches sought for engineering EV surfaces can be categorized as physical, chemical, and genetic engineering strategies. The choice of method depends on the specific application and desired outcome. Each has its advantages and disadvantages. This review lends a bird’s-eye view of the recent progress in these approaches with respect to their rational implications in the immunomodulation of tumor microenvironments (TME) from pro-tumorigenic to anti-tumorigenic ones. The strategies for modulating TME using targeted EVs, their advantages, current limitations, and future directions are discussed. Full article
(This article belongs to the Special Issue The Biological Mechanism of Cancer Proliferation and Metastasis)
►▼ Show Figures

Figure 1

20 pages, 2366 KiB  
Review
Biological Functions of the DNA Glycosylase NEIL3 and Its Role in Disease Progression Including Cancer
by Lang Chen, Xuan Huan, Xi-Dan Gao, Wu-Han Yu, Guo-Hui Xiao, Teng-Fei Li, Zhe-Yuan Wang and You-Cheng Zhang
Cancers 2022, 14(23), 5722; https://doi.org/10.3390/cancers14235722 - 22 Nov 2022
Cited by 3 | Viewed by 2081
Abstract
The accumulation of oxidative DNA base damage can severely disrupt the integrity of the genome and is strongly associated with the development of cancer. DNA glycosylase is the critical enzyme that initiates the base excision repair (BER) pathway, recognizing and excising damaged bases. [...] Read more.
The accumulation of oxidative DNA base damage can severely disrupt the integrity of the genome and is strongly associated with the development of cancer. DNA glycosylase is the critical enzyme that initiates the base excision repair (BER) pathway, recognizing and excising damaged bases. The Nei endonuclease VIII-like 3 (NEIL3) is an emerging DNA glycosylase essential in maintaining genome stability. With an in-depth study of the structure and function of NEIL3, we found that it has properties related to the process of base damage repair. For example, it not only prefers the base damage of single-stranded DNA (ssDNA), G-quadruplex and DNA interstrand crosslinks (ICLs), but also participates in the maintenance of replication fork stability and telomere integrity. In addition, NEIL3 is strongly associated with the progression of cancers and cardiovascular and neurological diseases, is incredibly significantly overexpressed in cancers, and may become an independent prognostic marker for cancer patients. Interestingly, circNEIL3, a circular RNA of exon-encoded origin by NEIL3, also promotes the development of multiple cancers. In this review, we have summarized the structure and the characteristics of NEIL3 to repair base damage. We have focused on NEIL3 and circNEIL3 in cancer development, progression and prognosis. Full article
(This article belongs to the Special Issue The Biological Mechanism of Cancer Proliferation and Metastasis)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-8
Back to TopTop