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Molecular Mechanisms of Cancer Progression and Targeted Therapy Attempts
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Molecular Mechanisms of Cancer Progression and Targeted Therapy Attempts

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 34107

Special Issue Editor

Prof. Dr. Daniela Taverna

E-Mail Website
Guest Editor
Molecular Biotechnology Center, Department of Molecular Biotechnology and Health Sciences, University of Turin, Via Nizza, 52-10126 Turin, Italy
Interests: microRNAs; adhesion molecules; tumor progression

Special Issue Information

Dear Colleagues,

Cancer is a multistep disease that can evolve into a metastatic stage which is among the leading causes of death worldwide. Primary tumor masses and metastases are composed of heterogeneous tumor cells and a surrounding tumor microenvironment (TME), including stroma cells and extracellular matrices (ECM). Many genes coding for proteins or not (microRNAs, long noncoding RNAs) have been found to be deregulated in cancer and stroma cells and impact cancer formation and spreading. In this Special Issue, we aim at collecting papers or reviews presenting the molecular mechanism of tumor progression related to tumor cells or to the interaction between tumor and stroma participants, focusing, in particular, on solid tumors. We also would like to collect different therapeutic interventions that can specifically target directly proteins or microRNAs or long noncoding RNAs.

Prof. Dr. Daniela Taverna
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • Tumor 
  • Metastasis 
  • Migration 
  • Noncoding RNAs 
  • Transcription factors 
  • Adhesion molecules 
  • Microenvironment 
  • Targeted therapy

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Published Papers (6 papers)

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Research

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18 pages, 3768 KiB  
Article
Picrasidine I Triggers Heme Oxygenase-1-Induced Apoptosis in Nasopharyngeal Carcinoma Cells via ERK and Akt Signaling Pathways
by Hsin-Yu Ho, Ping-Ju Chen, Yi-Ching Chuang, Yu-Sheng Lo, Chia-Chieh Lin, Ming-Ju Hsieh and Mu-Kuan Chen
Int. J. Mol. Sci. 2022, 23(11), 6103; https://doi.org/10.3390/ijms23116103 - 29 May 2022
Cited by 6 | Viewed by 2506
Abstract
Nasopharyngeal carcinoma (NPC) has a higher incidence in Taiwan than worldwide. Although it is a radiosensitive malignancy, cancer recurrence is still high in the advanced stages because of its ability to induce lymph node metastasis. Picrasidine I from Picrasma quassioides has been reported [...] Read more.
Nasopharyngeal carcinoma (NPC) has a higher incidence in Taiwan than worldwide. Although it is a radiosensitive malignancy, cancer recurrence is still high in the advanced stages because of its ability to induce lymph node metastasis. Picrasidine I from Picrasma quassioides has been reported as a potential drug for targeting multiple signaling pathways. The present study aimed to explore the role of picrasidine I in the apoptosis of NPC cells. Our results show that picrasidine I induced cytotoxic effects in NPC cells and caused cell cycle arrest in the sub-G1, S, and G2/M phases. Western blot analysis further demonstrated that the modulation of apoptosis through the extrinsic and intrinsic pathways was involved in picrasidine I-induced cell death. Downregulation of the ERK1/2 and Akt signaling pathways was also found in picrasidine I-induced apoptosis. Additionally, the apoptosis array showed that picrasidine I significantly increased heme oxygenase-1 (HO-1) expression, which could act as a critical molecule in picrasidine I-induced apoptosis in NPC cells. The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets also revealed that the HMOX1 mRNA level (HO-1) is lower in patients with head and neck squamous carcinoma (HNSCC) and NPC than in patients without cancer. Our study indicated that picrasidine I exerts anticancer effects in NPC by modulating HO-1 via the ERK and Akt signaling pathways. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer Progression and Targeted Therapy Attempts)
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18 pages, 10064 KiB  
Article
Patient-Derived Organoids of Cholangiocarcinoma
by Christopher Fabian Maier, Lei Zhu, Lahiri Kanth Nanduri, Daniel Kühn, Susan Kochall, May-Linn Thepkaysone, Doreen William, Konrad Grützmann, Barbara Klink, Johannes Betge, Jürgen Weitz, Nuh N. Rahbari, Christoph Reißfelder and Sebastian Schölch
Int. J. Mol. Sci. 2021, 22(16), 8675; https://doi.org/10.3390/ijms22168675 - 12 Aug 2021
Cited by 44 | Viewed by 8606
Abstract
Cholangiocarcinoma (CC) is an aggressive malignancy with an inferior prognosis due to limited systemic treatment options. As preclinical models such as CC cell lines are extremely rare, this manuscript reports a protocol of cholangiocarcinoma patient-derived organoid culture as well as a protocol for [...] Read more.
Cholangiocarcinoma (CC) is an aggressive malignancy with an inferior prognosis due to limited systemic treatment options. As preclinical models such as CC cell lines are extremely rare, this manuscript reports a protocol of cholangiocarcinoma patient-derived organoid culture as well as a protocol for the transition of 3D organoid lines to 2D cell lines. Tissue samples of non-cancer bile duct and cholangiocarcinoma were obtained during surgical resection. Organoid lines were generated following a standardized protocol. 2D cell lines were generated from established organoid lines following a novel protocol. Subcutaneous and orthotopic patient-derived xenografts were generated from CC organoid lines, histologically examined, and treated using standard CC protocols. Therapeutic responses of organoids and 2D cell lines were examined using standard CC agents. Next-generation exome and RNA sequencing was performed on primary tumors and CC organoid lines. Patient-derived organoids closely recapitulated the original features of the primary tumors on multiple levels. Treatment experiments demonstrated that patient-derived organoids of cholangiocarcinoma and organoid-derived xenografts can be used for the evaluation of novel treatments and may therefore be used in personalized oncology approaches. In summary, this study establishes cholangiocarcinoma organoids and organoid-derived cell lines, thus expanding translational research resources of cholangiocarcinoma. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer Progression and Targeted Therapy Attempts)
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19 pages, 4803 KiB  
Article
Human Primary Breast Cancer Stem Cells Are Characterized by Epithelial-Mesenchymal Plasticity
by Juliane Strietz, Stella S. Stepputtis, Marie Follo, Peter Bronsert, Elmar Stickeler and Jochen Maurer
Int. J. Mol. Sci. 2021, 22(4), 1808; https://doi.org/10.3390/ijms22041808 - 11 Feb 2021
Cited by 24 | Viewed by 3899
Abstract
Triple-negative breast cancer (TNBC) is one of the most aggressive subtypes of breast cancer, with only limited treatment options available. Recently, cancer stem cells (CSCs) have emerged as the potential drivers of tumor progression due to their ability to both self-renew and give [...] Read more.
Triple-negative breast cancer (TNBC) is one of the most aggressive subtypes of breast cancer, with only limited treatment options available. Recently, cancer stem cells (CSCs) have emerged as the potential drivers of tumor progression due to their ability to both self-renew and give rise to differentiated progeny. The CSC state has been linked to the process of epithelial-mesenchymal transition (EMT) and to the highly flexible state of epithelial-mesenchymal plasticity (EMP). We aimed to establish primary breast cancer stem cell (BCSC) cultures isolated from TNBC specimens. These cells grow as tumor spheres under anchorage-independent culture conditions in vitro and reliably form tumors in mice when transplanted in limiting dilutions in vivo. The BCSC xenograft tumors phenocopy the original patient tumor in architecture and gene expression. Analysis of an EMT-related marker profile revealed the concomitant expression of epithelial and mesenchymal markers suggesting an EMP state for BCSCs of TNBC. Furthermore, BCSCs were susceptible to stimulation with the EMT inducer TGF-β1, resulting in upregulation of mesenchymal genes and enhanced migratory abilities. Overall, primary BCSC cultures are a promising model close to the patient that can be used both in vitro and in vivo to address questions of BCSC biology and evaluate new treatment options for TNBC. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer Progression and Targeted Therapy Attempts)
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Review

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28 pages, 2794 KiB  
Review
Recent Advances of m6A Demethylases Inhibitors and Their Biological Functions in Human Diseases
by Yazhen You, Yundong Fu, Mingjie Huang, Dandan Shen, Bing Zhao, Hongmin Liu, Yichao Zheng and Lihua Huang
Int. J. Mol. Sci. 2022, 23(10), 5815; https://doi.org/10.3390/ijms23105815 - 22 May 2022
Cited by 48 | Viewed by 6184
Abstract
N6-methyladenosine (m6A) is a post-transcriptional RNA modification and one of the most abundant types of RNA chemical modifications. m6A functions as a molecular switch and is involved in a range of biomedical aspects, including cardiovascular diseases, the central nervous system, and cancers. Conceptually, [...] Read more.
N6-methyladenosine (m6A) is a post-transcriptional RNA modification and one of the most abundant types of RNA chemical modifications. m6A functions as a molecular switch and is involved in a range of biomedical aspects, including cardiovascular diseases, the central nervous system, and cancers. Conceptually, m6A methylation can be dynamically and reversibly modulated by RNA methylation regulatory proteins, resulting in diverse fates of mRNAs. This review focuses on m6A demethylases fat-mass- and obesity-associated protein (FTO) and alkB homolog 5 (ALKBH5), which especially erase m6A modification from target mRNAs. Recent advances have highlighted that FTO and ALKBH5 play an oncogenic role in various cancers, such as acute myeloid leukemias (AML), glioblastoma, and breast cancer. Moreover, studies in vitro and in mouse models confirmed that FTO-specific inhibitors exhibited anti-tumor effects in several cancers. Accumulating evidence has suggested the possibility of FTO and ALKBH5 as therapeutic targets for specific diseases. In this review, we aim to illustrate the structural properties of these two m6A demethylases and the development of their specific inhibitors. Additionally, this review will summarize the biological functions of these two m6A demethylases in various types of cancers and other human diseases. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer Progression and Targeted Therapy Attempts)
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28 pages, 6287 KiB  
Review
The Molecular Basis of Ubiquitin-Conjugating Enzymes (E2s) as a Potential Target for Cancer Therapy
by Xiaodi Du, Hongyu Song, Nengxing Shen, Ruiqi Hua and Guangyou Yang
Int. J. Mol. Sci. 2021, 22(7), 3440; https://doi.org/10.3390/ijms22073440 - 26 Mar 2021
Cited by 25 | Viewed by 6544
Abstract
Ubiquitin-conjugating enzymes (E2s) are one of the three enzymes required by the ubiquitin-proteasome pathway to connect activated ubiquitin to target proteins via ubiquitin ligases. E2s determine the connection type of the ubiquitin chains, and different types of ubiquitin chains regulate the stability and [...] Read more.
Ubiquitin-conjugating enzymes (E2s) are one of the three enzymes required by the ubiquitin-proteasome pathway to connect activated ubiquitin to target proteins via ubiquitin ligases. E2s determine the connection type of the ubiquitin chains, and different types of ubiquitin chains regulate the stability and activity of substrate proteins. Thus, E2s participate in the regulation of a variety of biological processes. In recent years, the importance of E2s in human health and diseases has been particularly emphasized. Studies have shown that E2s are dysregulated in variety of cancers, thus it might be a potential therapeutic target. However, the molecular basis of E2s as a therapeutic target has not been described systematically. We reviewed this issue from the perspective of the special position and role of E2s in the ubiquitin-proteasome pathway, the structure of E2s and biological processes they are involved in. In addition, the inhibitors and microRNAs targeting E2s are also summarized. This article not only provides a direction for the development of effective drugs but also lays a foundation for further study on this enzyme in the future. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer Progression and Targeted Therapy Attempts)
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24 pages, 5993 KiB  
Review
An Updated Focus on Quadruplex Structures as Potential Therapeutic Targets in Cancer
by Victoria Sanchez-Martin, Carmen Lopez-Pujante, Miguel Soriano-Rodriguez and Jose A. Garcia-Salcedo
Int. J. Mol. Sci. 2020, 21(23), 8900; https://doi.org/10.3390/ijms21238900 - 24 Nov 2020
Cited by 26 | Viewed by 5353
Abstract
Non-canonical, four-stranded nucleic acids secondary structures are present within regulatory regions in the human genome and transcriptome. To date, these quadruplex structures include both DNA and RNA G-quadruplexes, formed in guanine-rich sequences, and i-Motifs, found in cytosine-rich sequences, as their counterparts. Quadruplexes have [...] Read more.
Non-canonical, four-stranded nucleic acids secondary structures are present within regulatory regions in the human genome and transcriptome. To date, these quadruplex structures include both DNA and RNA G-quadruplexes, formed in guanine-rich sequences, and i-Motifs, found in cytosine-rich sequences, as their counterparts. Quadruplexes have been extensively associated with cancer, playing an important role in telomere maintenance and control of genetic expression of several oncogenes and tumor suppressors. Therefore, quadruplex structures are considered attractive molecular targets for cancer therapeutics with novel mechanisms of action. In this review, we provide a general overview about recent research on the implications of quadruplex structures in cancer, firstly gathering together DNA G-quadruplexes, RNA G-quadruplexes as well as DNA i-Motifs. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Cancer Progression and Targeted Therapy Attempts)
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