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Cancers
Special Issues
Molecular Mechanisms of Cancer Development and Metastasis
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Molecular Mechanisms of Cancer Development and Metastasis

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

Deadline for manuscript submissions: 20 December 2024 | Viewed by 11165

Special Issue Editors

Dr. Babak Behnam

E-Mail
Guest Editor
Department of Regulatory Affairs, Amarex Clinical Research, NSF International, Germantown, MD 20874, USA
Interests: cancer genetics; tumor biology; cancer stem cell; clinical genetics; molecular biology; cell organelles
Dr. Hassan Fazilaty

E-Mail Website
Guest Editor
Department of Molecular Life Sciences, University of Zurich, 8006 Zurich, Switzerland
Interests: molecular biology; cancer biology; developmental biology; epithelial to mesenchymal transition (EMT); regeneration

Special Issue Information

Dear Colleagues,

The spread of cancer cells, a process called metastasis, is the main reason for the majority of cancer-related deaths, and most current therapies are incapable of efficiently treating metastatic cancers. This is due to our lack of understanding of the complex biological process that occurs during metastasis. Therefore, the comprehensive identification of molecular mechanisms underlying cancer development and metastasis is essential to devise new therapies. 

This Special Issue refers to the underlying biological processes that lead to the development and spread of cancer cells; the key areas include genetic and nongenetic molecular alterations, dysregulated signaling pathways, angiogenesis, cell migration and invasion, epithelial-to-mesenchymal transition (EMT) and immune system evasion. 

Dr. Babak Behnam
Dr. Hassan Fazilaty
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

  • cancer microenvironment
  • metastatic pathway
  • cancer stem cell
  • Epithelial-to-mesenchymal transition
  • EMT
  • Cell invasion
  • Immune evasion
  • Cell plasticity
  • Cell migration

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Published Papers (8 papers)

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Research

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16 pages, 42416 KiB  
Article
FBXO11 Mediates Ubiquitination of ZEB1 and Modulates Epithelial-to-Mesenchymal Transition in Lung Cancer Cells
by Xinyue Zhao, Zhihui Han, Ruiying Liu, Zehao Li, Ling Mei and Yue Jin
Cancers 2024, 16(19), 3269; https://doi.org/10.3390/cancers16193269 - 26 Sep 2024
Viewed by 736
Abstract
Epithelial-to-mesenchymal transition (EMT) affects the invasion and migration of cancer cells. Here, we show that FBXO11 recognizes and promotes ubiquitin-mediated degradation of ZEB1. There is a strong association between FBXO11 and ZEB1 in non-small cell lung cancer (NSLC) in a clinical database. FBXO11 [...] Read more.
Epithelial-to-mesenchymal transition (EMT) affects the invasion and migration of cancer cells. Here, we show that FBXO11 recognizes and promotes ubiquitin-mediated degradation of ZEB1. There is a strong association between FBXO11 and ZEB1 in non-small cell lung cancer (NSLC) in a clinical database. FBXO11 interacts with ZEB1, a core inducer of EMT. FBXO11 leads to increased ubiquitination and proteasomal degradation of ZEB1. Depletion of endogenous FBXO11 causes ZEB1 protein accumulation and EMT in A549 and H1299 cells, while overexpression of FBXO11 reduces ZEB1 protein abundance and cellular invasiveness. Importantly, the depletion of ZEB1 suppresses the increased migration and invasion of A549 and H1299 cells promoted by the depletion of FBXO11. The same results are shown in xenograft tumors. High FBXO11 expression is associated with a favorable prognosis in NSLC. Collectively, our study demonstrates that FBXO11 modulates EMT by mediating the stability of ZEB1 in lung cancer cells. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer Development and Metastasis)
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19 pages, 4358 KiB  
Article
Fasting-Mimicking Diet Inhibits Autophagy and Synergizes with Chemotherapy to Promote T-Cell-Dependent Leukemia-Free Survival
by Roberta Buono, Jonathan Tucci, Raffaello Cutri, Novella Guidi, Serghei Mangul, Franca Raucci, Matteo Pellegrini, Steven D. Mittelman and Valter D. Longo
Cancers 2023, 15(24), 5870; https://doi.org/10.3390/cancers15245870 - 16 Dec 2023
Cited by 1 | Viewed by 2318
Abstract
Fasting mimicking diets (FMDs) are effective in the treatment of many solid tumors in mouse models, but their effect on hematologic malignancies is poorly understood, particularly in combination with standard therapies. Here we show that cycles of a 3-day FMD given to high-fat-diet-fed [...] Read more.
Fasting mimicking diets (FMDs) are effective in the treatment of many solid tumors in mouse models, but their effect on hematologic malignancies is poorly understood, particularly in combination with standard therapies. Here we show that cycles of a 3-day FMD given to high-fat-diet-fed mice once a week increased the efficacy of vincristine to improve survival from BCR-ABL B acute lymphoblastic leukemia (ALL). In mice fed a standard diet, FMD cycles in combination with vincristine promoted cancer-free survival. RNA seq and protein assays revealed a vincristine-dependent decrease in the expression of multiple autophagy markers, which was exacerbated by the fasting/FMD conditions. The autophagy inhibitor chloroquine could substitute for fasting/FMD to promote cancer-free survival in combination with vincristine. In vitro, targeted inhibition of autophagy genes ULK1 and ATG9a strongly potentiated vincristine’s toxicity. Moreover, anti-CD8 antibodies reversed the effects of vincristine plus fasting/FMD in promoting leukemia-free survival in mice, indicating a central role of the immune system in this response. Thus, the inhibition of autophagy and enhancement of immune responses appear to be mediators of the fasting/FMD-dependent cancer-free survival in ALL mice. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer Development and Metastasis)
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21 pages, 3945 KiB  
Article
AKT2 Loss Impairs BRAF-Mutant Melanoma Metastasis
by Siobhan K. McRee, Abraham L. Bayer, Jodie Pietruska, Philip N. Tsichlis and Philip W. Hinds
Cancers 2023, 15(20), 4958; https://doi.org/10.3390/cancers15204958 - 12 Oct 2023
Cited by 2 | Viewed by 1352
Abstract
Despite recent advances in treatment, melanoma remains the deadliest form of skin cancer due to its highly metastatic nature. Melanomas harboring oncogenic BRAFV600E mutations combined with PTEN loss exhibit unrestrained PI3K/AKT signaling and increased invasiveness. However, the contribution of different AKT isoforms [...] Read more.
Despite recent advances in treatment, melanoma remains the deadliest form of skin cancer due to its highly metastatic nature. Melanomas harboring oncogenic BRAFV600E mutations combined with PTEN loss exhibit unrestrained PI3K/AKT signaling and increased invasiveness. However, the contribution of different AKT isoforms to melanoma initiation, progression, and metastasis has not been comprehensively explored, and questions remain about whether individual isoforms play distinct or redundant roles in each step. We investigate the contribution of individual AKT isoforms to melanoma initiation using a novel mouse model of AKT isoform-specific loss in a murine melanoma model, and we investigate tumor progression, maintenance, and metastasis among a panel of human metastatic melanoma cell lines using AKT isoform-specific knockdown studies. We elucidate that AKT2 is dispensable for primary tumor formation but promotes migration and invasion in vitro and metastatic seeding in vivo, whereas AKT1 is uniquely important for melanoma initiation and cell proliferation. We propose a mechanism whereby the inhibition of AKT2 impairs glycolysis and reduces an EMT-related gene expression signature in PTEN-null BRAF-mutant human melanoma cells to limit metastatic spread. Our data suggest that the elucidation of AKT2-specific functions in metastasis might inform therapeutic strategies to improve treatment options for melanoma patients. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer Development and Metastasis)
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19 pages, 5799 KiB  
Article
TCF12 Activates TGFB2 Expression to Promote the Malignant Progression of Melanoma
by Youjia Tian, Jiang Zhou, Xinxin Chai, Zejun Ping, Yurong Zhao, Xin Xu, Chi Luo and Jinghao Sheng
Cancers 2023, 15(18), 4505; https://doi.org/10.3390/cancers15184505 - 11 Sep 2023
Cited by 3 | Viewed by 1565
Abstract
As one of the most common malignant tumors, melanoma is a serious threat to human health. More than half of melanoma patients have a BRAF mutation, and 90% of them have a BRAF(V600E) mutation. There is a targeted therapy for patients using a [...] Read more.
As one of the most common malignant tumors, melanoma is a serious threat to human health. More than half of melanoma patients have a BRAF mutation, and 90% of them have a BRAF(V600E) mutation. There is a targeted therapy for patients using a BRAF(V600E) inhibitor. However, no response to treatment is generally inevitable due to the heterogeneity of melanoma. Coupled with its high metastatic character, melanoma ultimately leads to poor overall survival. This study aimed to explore the possible mechanisms of melanoma metastasis and identify a more effective method for the treatment of melanoma. In this paper, we report that TCF12 expression is higher in melanoma, especially in metastatic tumors, through analyzing data from TCGA. Then, cell proliferation, colony formation, and transwell assays show that the upregulated expression of TCF12 can promote proliferation and metastasis of melanoma cells in vitro. The same result is confirmed in the subcutaneous tumor formation assay. Moreover, TGFB2 is identified as a direct downstream target of TCF12 by RNA-seq, qPCR, immunoblotting, ChIP, and a dual luciferase reporting assay. Interestingly, depletion of TCF12 can sensitize melanoma to BRAF inhibition both in vitro and in vivo. Overall, our results demonstrate that TCF12 promotes melanoma progression and can be a potential tumor therapeutic target. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer Development and Metastasis)
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Review

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15 pages, 5975 KiB  
Review
Emerging Paradigms in Cancer Metastasis: Ghost Mitochondria, Vasculogenic Mimicry, and Polyploid Giant Cancer Cells
by Mateusz Krotofil, Maciej Tota, Jakub Siednienko and Piotr Donizy
Cancers 2024, 16(20), 3539; https://doi.org/10.3390/cancers16203539 - 19 Oct 2024
Viewed by 668
Abstract
The capacity of cancer cells to migrate from a primary tumor, disseminate throughout the body, and eventually establish secondary tumors is a fundamental aspect of metastasis. A detailed understanding of the cellular and molecular mechanisms underpinning this multifaceted process would facilitate the rational [...] Read more.
The capacity of cancer cells to migrate from a primary tumor, disseminate throughout the body, and eventually establish secondary tumors is a fundamental aspect of metastasis. A detailed understanding of the cellular and molecular mechanisms underpinning this multifaceted process would facilitate the rational development of therapies aimed at treating metastatic disease. Although various hypotheses and models have been proposed, no single concept fully explains the mechanism of metastasis or integrates all observations and experimental findings. Recent advancements in metastasis research have refined existing theories and introduced new ones. This review evaluates several novel/emerging theories, focusing on ghost mitochondria (GM), vasculogenic mimicry (VM), and polyploid giant cancer cells (PGCCs). Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer Development and Metastasis)
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16 pages, 1997 KiB  
Review
Exploring TSGA10 Function: A Crosstalk or Controlling Mechanism in the Signaling Pathway of Carcinogenesis?
by Farzad Taghizadeh-Hesary, Mobina Ghadyani, Fatah Kashanchi and Babak Behnam
Cancers 2024, 16(17), 3044; https://doi.org/10.3390/cancers16173044 - 31 Aug 2024
Viewed by 696
Abstract
Cancer-specific antigens have been a significant area of focus in cancer treatment since their discovery in the mid-twentieth century. Cancer germline antigens are a class of antigens specifically overexpressed in germline tissues and cancer cells. Among these, TSGA10 (testis-specific gene antigen 10) is [...] Read more.
Cancer-specific antigens have been a significant area of focus in cancer treatment since their discovery in the mid-twentieth century. Cancer germline antigens are a class of antigens specifically overexpressed in germline tissues and cancer cells. Among these, TSGA10 (testis-specific gene antigen 10) is of great interest because of its crucial impact on cancer progression. Early studies explored TSGA10 expression in a variety of cancer types. More recent studies revealed that TSGA10 can suppress tumor progression by blocking cancer cell metabolism, angiogenesis, and metastasis. An open question regarding the TSGA10 is why cancer cells must express a protein that prevents their progression. To answer this question, we conducted a comprehensive review to engage the TSGA10 in the context of the current understanding of “malignant transformation”. This review demonstrated that TSGA10 expression level in cancer cells depends on the cancer stage across malignant transformation. In addition, we evaluated how TSGA10 expression can prevent the “cancer hallmarks”. Given this information, TSGA10 can be of great interest in developing effective targeted anti-cancer therapies. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer Development and Metastasis)
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13 pages, 885 KiB  
Review
Immune Response and Metastasis—Links between the Metastasis Driver MACC1 and Cancer Immune Escape Strategies
by Sebastian Torke, Wolfgang Walther and Ulrike Stein
Cancers 2024, 16(7), 1330; https://doi.org/10.3390/cancers16071330 - 28 Mar 2024
Cited by 1 | Viewed by 1223
Abstract
Metastasis remains the most critical factor limiting patient survival and the most challenging part of cancer-targeted therapy. Identifying the causal drivers of metastasis and characterizing their properties in various key aspects of cancer biology is essential for the development of novel metastasis-targeting approaches. [...] Read more.
Metastasis remains the most critical factor limiting patient survival and the most challenging part of cancer-targeted therapy. Identifying the causal drivers of metastasis and characterizing their properties in various key aspects of cancer biology is essential for the development of novel metastasis-targeting approaches. Metastasis-associated in colon cancer 1 (MACC1) is a prognostic and predictive biomarker that is now recognized in more than 20 cancer entities. Although MACC1 can already be linked with many hallmarks of cancer, one key process—the facilitation of immune evasion—remains poorly understood. In this review, we explore the direct and indirect links between MACC1 and the mechanisms of immune escape. Therein, we highlight the signaling pathways and secreted factors influenced by MACC1 as well as their effects on the infiltration and anti-tumor function of immune cells. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer Development and Metastasis)
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27 pages, 4011 KiB  
Review
Dual Functions of T Lymphocytes in Breast Carcinoma: From Immune Protection to Orchestrating Tumor Progression and Metastasis
by Mohammadrasul Zareinejad, Fereshteh Mehdipour, Mina Roshan-Zamir, Zahra Faghih and Abbas Ghaderi
Cancers 2023, 15(19), 4771; https://doi.org/10.3390/cancers15194771 - 28 Sep 2023
Cited by 8 | Viewed by 1691
Abstract
Breast cancer (BC) is the most common cancer type in women and the second leading cause of death. Despite recent advances, the mortality rate of BC is still high, highlighting a need to develop new treatment strategies including the modulation of the immune [...] Read more.
Breast cancer (BC) is the most common cancer type in women and the second leading cause of death. Despite recent advances, the mortality rate of BC is still high, highlighting a need to develop new treatment strategies including the modulation of the immune system and immunotherapies. In this regard, understanding the complex function of the involved immune cells and their crosstalk with tumor cells is of great importance. T-cells are recognized as the most important cells in the tumor microenvironment and are divided into several subtypes including helper, cytotoxic, and regulatory T-cells according to their transcription factors, markers, and functions. This article attempts to provide a comprehensive review of the role of T-cell subsets in the prognosis and treatment of patients with BC, and crosstalk between tumor cells and T-cells. The literature overwhelmingly contains controversial findings mainly due to the plasticity of T-cell subsets within the inflammatory conditions and the use of different panels for their phenotyping. However, investigating the role of T-cells in BC immunity depends on a variety of factors including tumor types or subtypes, the stage of the disease, the localization of the cells in the tumor tissue and the presence of different cells or cytokines. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer Development and Metastasis)
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