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Advances in Molecular Research of Oncogenes

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 (31 October 2022) | Viewed by 37526

Special Issue Editors

Dr. Eugenio Santos

E-Mail Website
Guest Editor
Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer (CSIC-Universidad de Salamanca) and CIBERONC, 37007 Salamanca, Spain
Interests: RAS oncogenes; RAS signaling pathways; RAS activation by guanine nucleotide exchange factors (GEFs); mammalian GEFs of the SOS and GRF families; inhibitors of RAS-driven tumors; cancer molecular biology; signal transduction
Special Issues, Collections and Topics in MDPI journals
Dr. Fernando C. Baltanás

E-Mail Website
Guest Editor
CIC-IBMCC, Universidad de Salamanca-CSIC and CIBERONC, 37007 Salamanca, Spain
Interests: Ras signaling; Son of sevenless; Sos1; Sos2; GEF; neurodegeneration

Special Issue Information

Dear Colleagues,

It has been over forty years since the isolation of the first human oncogene, a critical breakthrough in cancer research. Since then, the identification of new pathogenic oncogenes has continuously grown. The detailed characterization of how oncogenes dysregulate signaling pathways controlling many cellular important physiological processes, triggering developmental syndromes or many cancer types, as well as the discovery of novel small-molecule inhibitors able to block, or at least attenuate, oncogene mode of action appear as the new steps forward in our understanding of cancer research in the following years.

The purpose of this Special Issue is to explore the expanding field of molecular research of Oncogenes to provide valuable translational clues that can help in anticipating relevant clinical needs.

Dr. Eugenio Santos
Dr. Fernando C. Baltanás
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 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

  • oncogene toxicity
  • cancer
  • signaling pathways
  • signal transduction
  • small-molecule inhibitors
  • resistance mechanisms
  • molecular therapy
  • protein–protein interaction
  • therapeutic targets
  • cell signaling

Published Papers (12 papers)

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Editorial

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2 pages, 185 KiB  
Editorial
Advances in Molecular Research of Oncogenes
by Fernando C. Baltanas and Eugenio Santos
Int. J. Mol. Sci. 2023, 24(8), 7222; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24087222 - 13 Apr 2023
Viewed by 880
Abstract
The isolation of the first human oncogene (HRAS), a critical breakthrough in cancer research, has occurred over forty years ago, and the identification of new pathogenic oncogenes has continuously grown since [...] Full article
(This article belongs to the Special Issue Advances in Molecular Research of Oncogenes)

Research

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17 pages, 2942 KiB  
Article
The 3q Oncogene SEC62 Predicts Response to Neoadjuvant Chemotherapy and Regulates Tumor Cell Migration in Triple Negative Breast Cancer
by Julia C. Radosa, Mariz Kasoha, Merle Doerk, Annika Cullmann, Askin C. Kaya, Maximilian Linxweiler, Marc P. Radosa, Zoltan Takacs, Andrea Tirincsi, Sven Lang, Martin Jung, Julian Puppe, Barbara Linxweiler, Mathias Wagner, Rainer M. Bohle, Erich-Franz Solomayer and Julia S. M. Zimmermann
Int. J. Mol. Sci. 2023, 24(11), 9576; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24119576 - 31 May 2023
Cited by 1 | Viewed by 1188
Abstract
In the absence of targeted treatment options, neoadjuvant chemotherapy (NACT) is applied widely for triple-negative breast cancer (TNBC). Response to NACT is an important parameter predictive of oncological outcomes (progression-free and overall survival). An approach to the evaluation of predictive markers enabling therapy [...] Read more.
In the absence of targeted treatment options, neoadjuvant chemotherapy (NACT) is applied widely for triple-negative breast cancer (TNBC). Response to NACT is an important parameter predictive of oncological outcomes (progression-free and overall survival). An approach to the evaluation of predictive markers enabling therapy individualization is the identification of tumor driver genetic mutations. This study was conducted to investigate the role of SEC62, harbored at 3q26 and identified as a driver of breast cancer pathogenesis, in TNBC. We analyzed SEC62 expression in The Cancer Genome Atlas database, and immunohistologically investigated SEC62 expression in pre- and post-NACT tissue samples from 64 patients with TNBC treated at the Department of Gynecology and Obstetrics/Saarland University Hospital/Homburg between January 2010 and December 2018 and compared the effect of SEC62 on tumor cell migration and proliferation in functional assays. SEC62 expression dynamics correlated positively with the response to NACT (p ≤ 0.01) and oncological outcomes (p ≤ 0.01). SEC62 expression stimulated tumor cell migration (p ≤ 0.01). The study findings indicate that SEC62 is overexpressed in TNBC and serves as a predictive marker for the response to NACT, a prognostic marker for oncological outcomes, and a migration-stimulating oncogene in TNBC. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Oncogenes)
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18 pages, 2880 KiB  
Article
α4-α5 Helices on Surface of KRAS Can Accommodate Small Compounds That Increase KRAS Signaling While Inducing CRC Cell Death
by Baraa Abuasaker, Eduardo Garrido, Marta Vilaplana, Jesús Daniel Gómez-Zepeda, Sonia Brun, Marta Garcia-Cajide, Caroline Mauvezin, Montserrat Jaumot, Maria Dolors Pujol, Jaime Rubio-Martínez and Neus Agell
Int. J. Mol. Sci. 2023, 24(1), 748; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24010748 - 01 Jan 2023
Cited by 2 | Viewed by 2169
Abstract
KRAS is the most frequently mutated oncogene associated with the genesis and progress of pancreatic, lung and colorectal (CRC) tumors. KRAS has always been considered as a therapeutic target in cancer but until now only two compounds that inhibit one specific KRAS mutation [...] Read more.
KRAS is the most frequently mutated oncogene associated with the genesis and progress of pancreatic, lung and colorectal (CRC) tumors. KRAS has always been considered as a therapeutic target in cancer but until now only two compounds that inhibit one specific KRAS mutation have been approved for clinical use. In this work, by molecular dynamics and a docking process, we describe a new compound (P14B) that stably binds to a druggable pocket near the α4-α5 helices of the allosteric domain of KRAS. This region had previously been identified as the binding site for calmodulin (CaM). Using surface plasmon resonance and pulldown analyses, we prove that P14B binds directly to oncogenic KRAS thus competing with CaM. Interestingly, P14B favors oncogenic KRAS interaction with BRAF and phosphorylated C-RAF, and increases downstream Ras signaling in CRC cells expressing oncogenic KRAS. The viability of these cells, but not that of the normal cells, is impaired by P14B treatment. These data support the significance of the α4-α5 helices region of KRAS in the regulation of oncogenic KRAS signaling, and demonstrate that drugs interacting with this site may destine CRC cells to death by increasing oncogenic KRAS downstream signaling. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Oncogenes)
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17 pages, 5282 KiB  
Article
PEBP4 Directs the Malignant Behavior of Hepatocellular Carcinoma Cells via Regulating mTORC1 and mTORC2
by Qiongfeng Chen, Jingguang Jin, Wenhui Guo, Zhimin Tang, Yunfei Luo, Ying Ying, Hui Lin and Zhijun Luo
Int. J. Mol. Sci. 2022, 23(15), 8798; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23158798 - 08 Aug 2022
Cited by 4 | Viewed by 1743
Abstract
Phosphatidylethanolamine binding protein 4 (PEBP4) is an understudied multifunctional small protein. Previous studies have shown that the expression of PEBP4 is increased in many cancer specimens, which correlates to cancer progression. The present study explored the mechanism by which PEBP4 regulates the growth [...] Read more.
Phosphatidylethanolamine binding protein 4 (PEBP4) is an understudied multifunctional small protein. Previous studies have shown that the expression of PEBP4 is increased in many cancer specimens, which correlates to cancer progression. The present study explored the mechanism by which PEBP4 regulates the growth and progression of hepatocellular carcinoma cells. Thus, we showed that knockdown of PEBP4 in MHCC97H cells, where its expression was relatively high, diminished activities of serine/threonine protein kinase B (PKB, also known as Akt), mammalian target of rapamycin complex 1(mTORC1), and mTORC2, events that were not restored by insulin-like growth factor 1 (IGF-1). Conversely, overexpression of PEBP4 in MHCC97L cells with the low endogenous level yielded opposite effects. Furthermore, physical association of PEBP4 with Akt, mTORC1, and mTORC2 was observed. Interestingly, introduction of AktS473D mutant, bypassing phosphorylation by mTORC2, rescued mTORC1 activity, but without effects on mTORC2 signaling. In contrast, the effect of PEBP4 overexpression on the activity of mTORC1 but not that of mTORC2 was suppressed by MK2206, a specific inhibitor of Akt. In conjunction, PEBP4 knockdown-engendered reduction of cell proliferation, migration and invasion was partially rescued by Akt S473D while increases in these parameters induced by overexpression of PEBP4 were completely abolished by MK2206, although the expression of epithelial mesenchymal transition (EMT) markers appeared to be fully regulated by the active mutant of Akt. Finally, knockdown of PEBP4 diminished the growth of tumor and metastasis, whereas they were enhanced by overexpression of PEBP4. Altogether, our study suggests that increased expression of PEBP4 exacerbates malignant behaviors of hepatocellular cancer cells through cooperative participation of mTORC1 and mTORC2. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Oncogenes)
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16 pages, 14297 KiB  
Article
Thermal Shift Assay for Small GTPase Stability Screening: Evaluation and Suitability
by Kari Kopra, Salla Valtonen, Randa Mahran, Jonas N. Kapp, Nazia Hassan, William Gillette, Bryce Dennis, Lianbo Li, Kenneth D. Westover, Andreas Plückthun and Harri Härmä
Int. J. Mol. Sci. 2022, 23(13), 7095; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23137095 - 26 Jun 2022
Cited by 10 | Viewed by 4281
Abstract
Thermal unfolding methods are commonly used as a predictive technique by tracking the protein’s physical properties. Inherent protein thermal stability and unfolding profiles of biotherapeutics can help to screen or study potential drugs and to find stabilizing or destabilizing conditions. Differential scanning calorimetry [...] Read more.
Thermal unfolding methods are commonly used as a predictive technique by tracking the protein’s physical properties. Inherent protein thermal stability and unfolding profiles of biotherapeutics can help to screen or study potential drugs and to find stabilizing or destabilizing conditions. Differential scanning calorimetry (DSC) is a ‘Gold Standard’ for thermal stability assays (TSA), but there are also a multitude of other methodologies, such as differential scanning fluorimetry (DSF). The use of an external probe increases the assay throughput, making it more suitable for screening studies, but the current methodologies suffer from relatively low sensitivity. While DSF is an effective tool for screening, interpretation and comparison of the results is often complicated. To overcome these challenges, we compared three thermal stability probes in small GTPase stability studies: SYPRO Orange, 8-anilino-1-naphthalenesulfonic acid (ANS), and the Protein-Probe. We studied mainly KRAS, as a proof of principle to obtain biochemical knowledge through TSA profiles. We showed that the Protein-Probe can work at lower concentration than the other dyes, and its sensitivity enables effective studies with non-covalent and covalent drugs at the nanomolar level. Using examples, we describe the parameters, which must be taken into account when characterizing the effect of drug candidates, of both small molecules and Designed Ankyrin Repeat Proteins. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Oncogenes)
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16 pages, 3894 KiB  
Article
CRISPR/Cas9-Directed Gene Trap Constitutes a Selection System for Corrected BCR/ABL Leukemic Cells in CML
by Elena Vuelta, José L. Ordoñez, David J. Sanz, Sandra Ballesteros, Jesús M. Hernández-Rivas, Lucía Méndez-Sánchez, Manuel Sánchez-Martín and Ignacio García-Tuñón
Int. J. Mol. Sci. 2022, 23(12), 6386; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23126386 - 07 Jun 2022
Cited by 3 | Viewed by 2281
Abstract
Chronic myeloid leukaemia (CML) is a haematological neoplasm driven by the BCR/ABL fusion oncogene. The monogenic aspect of the disease and the feasibility of ex vivo therapies in haematological disorders make CML an excellent candidate for gene therapy strategies. The ability to abolish [...] Read more.
Chronic myeloid leukaemia (CML) is a haematological neoplasm driven by the BCR/ABL fusion oncogene. The monogenic aspect of the disease and the feasibility of ex vivo therapies in haematological disorders make CML an excellent candidate for gene therapy strategies. The ability to abolish any coding sequence by CRISPR-Cas9 nucleases offers a powerful therapeutic opportunity to CML patients. However, a definitive cure can only be achieved when only CRISPR-edited cells are selected. A gene-trapping approach combined with CRISPR technology would be an ideal approach to ensure this. Here, we developed a CRISPR-Trap strategy that efficiently inserts a donor gene trap (SA-CMV-Venus) cassette into the BCR/ABL-specific fusion point in the CML K562 human cell line. The trapping cassette interrupts the oncogene coding sequence and expresses a reporter gene that enables the selection of edited cells. Quantitative mRNA expression analyses showed significantly higher level of expression of the BCR/Venus allele coupled with a drastically lower level of BCR/ABL expression in Venus+ cell fractions. Functional in vitro experiments showed cell proliferation arrest and apoptosis in selected Venus+ cells. Finally, xenograft experiments with the selected Venus+ cells showed a large reduction in tumour growth, thereby demonstrating a therapeutic benefit in vivo. This study represents proof of concept for the therapeutic potential of a CRISPR-Trap system as a novel strategy for gene elimination in haematological neoplasms. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Oncogenes)
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Review

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30 pages, 3865 KiB  
Review
What Genetics Can Do for Oncological Imaging: A Systematic Review of the Genetic Validation Data Used in Radiomics Studies
by Rebeca Mirón Mombiela, Anne Rix Arildskov, Frederik Jager Bruun, Lotte Harries Hasselbalch, Kristine Bærentz Holst, Sine Hvid Rasmussen and Consuelo Borrás
Int. J. Mol. Sci. 2022, 23(12), 6504; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23126504 - 10 Jun 2022
Cited by 2 | Viewed by 2203
Abstract
(1) Background: Radiogenomics is motivated by the concept that biomedical images contain information that reflects underlying pathophysiology. This review focused on papers that used genetics to validate their radiomics models and outcomes and assess their contribution to this emerging field. (2) Methods: All [...] Read more.
(1) Background: Radiogenomics is motivated by the concept that biomedical images contain information that reflects underlying pathophysiology. This review focused on papers that used genetics to validate their radiomics models and outcomes and assess their contribution to this emerging field. (2) Methods: All original research with the words radiomics and genomics in English and performed in humans up to 31 January 2022, were identified on Medline and Embase. The quality of the studies was assessed with Radiomic Quality Score (RQS) and the Cochrane recommendation for diagnostic accuracy study Quality Assessment 2. (3) Results: 45 studies were included in our systematic review, and more than 50% were published in the last two years. The studies had a mean RQS of 12, and the studied tumors were very diverse. Up to 83% investigated the prognosis as the main outcome, with the rest focusing on response to treatment and risk assessment. Most applied either transcriptomics (54%) and/or genetics (35%) for genetic validation. (4) Conclusions: There is enough evidence to state that new science has emerged, focusing on establishing an association between radiological features and genomic/molecular expression to explain underlying disease mechanisms and enhance prognostic, risk assessment, and treatment response radiomics models in cancer patients. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Oncogenes)
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15 pages, 916 KiB  
Review
MYD88 Mutations: Transforming the Landscape of IgM Monoclonal Gammopathies
by Miguel Alcoceba, María García-Álvarez, Alejandro Medina, Rebeca Maldonado, Verónica González-Calle, María Carmen Chillón, María Eugenia Sarasquete, Marcos González, Ramón García-Sanz and Cristina Jiménez
Int. J. Mol. Sci. 2022, 23(10), 5570; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23105570 - 16 May 2022
Cited by 14 | Viewed by 4965
Abstract
The MYD88 gene has a physiological role in the innate immune system. Somatic mutations in MYD88, including the most common L265P, have been associated with the development of certain types of lymphoma. MYD88L265P is present in more than 90% of patients [...] Read more.
The MYD88 gene has a physiological role in the innate immune system. Somatic mutations in MYD88, including the most common L265P, have been associated with the development of certain types of lymphoma. MYD88L265P is present in more than 90% of patients with Waldenström’s macroglobulinemia (WM) and IgM monoclonal gammopathy of undetermined significance (IgM-MGUS). The absence of MYD88 mutations in WM patients has been associated with a higher risk of transformation into aggressive lymphoma, resistance to certain therapies (BTK inhibitors), and shorter overall survival. The MyD88 signaling pathway has also been used as a target for specific therapies. In this review, we summarize the clinical applications of MYD88 testing in the diagnosis, prognosis, follow-up, and treatment of patients. Although MYD88L265P is not specific to WM, few tumors present a single causative mutation in a recurrent position. The role of the oncogene in the pathogenesis of WM is still unclear, especially considering that the mutation can be found in normal B cells of patients, as recently reported. This may have important implications for early lymphoma detection in healthy elderly individuals and for the treatment response assessment based on a MYD88L265P analysis. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Oncogenes)
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26 pages, 1059 KiB  
Review
Role of the Ghrelin System in Colorectal Cancer
by Aldona Kasprzak
Int. J. Mol. Sci. 2022, 23(10), 5380; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23105380 - 11 May 2022
Cited by 9 | Viewed by 2578
Abstract
The ghrelin system contains several components (e.g., ghrelin with growing number of alternative peptides, growth hormone secretagogue receptors (GHS-Rs), and ghrelin-O-acyl-transferase (GOAT) and participates in regulation of a number of key processes of gastrointestinal (GI) tract cancer progression, including cell proliferation, migration, invasion, [...] Read more.
The ghrelin system contains several components (e.g., ghrelin with growing number of alternative peptides, growth hormone secretagogue receptors (GHS-Rs), and ghrelin-O-acyl-transferase (GOAT) and participates in regulation of a number of key processes of gastrointestinal (GI) tract cancer progression, including cell proliferation, migration, invasion, apoptosis, inflammation, and angiogenesis. However, its exact role in promoting or inhibiting cancer progression is still unclear. Colorectal cancer (CRC) is one of the most common human malignancies worldwide. Molecular studies suggest an autocrine/paracrine mechanism for the secretion of ghrelin in colorectal carcinogenesis and its contribution to its initial stages. However, the signalling pathways of CRC development involving the ghrelin system are poorly understood. Potential mechanisms of colon carcinogenesis involving components of the ghrelin system were previously described in an animal model and in in vitro studies. However, the diagnostic–prognostic role of serum ghrelin concentrations, tissue expression, or genetic changes of this system in various stages of CRC progression remains an open case. Thus, the aim of this study is to discuss the role of the ghrelin system in colon carcinogenesis, diagnostics and CRC prognostics, as well as the results of studies on the use of ghrelin and its analogues in the therapy of CRC-related syndromes (e.g., cachexia and sarcopenia). Full article
(This article belongs to the Special Issue Advances in Molecular Research of Oncogenes)
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27 pages, 2062 KiB  
Review
Transposable Elements and Human Diseases: Mechanisms and Implication in the Response to Environmental Pollutants
by Benoît Chénais
Int. J. Mol. Sci. 2022, 23(5), 2551; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23052551 - 25 Feb 2022
Cited by 20 | Viewed by 6041
Abstract
Transposable elements (TEs) are recognized as major players in genome plasticity and evolution. The high abundance of TEs in the human genome, especially the Alu and Long Interspersed Nuclear Element-1 (LINE-1) repeats, makes them responsible for the molecular origin of several diseases. This [...] Read more.
Transposable elements (TEs) are recognized as major players in genome plasticity and evolution. The high abundance of TEs in the human genome, especially the Alu and Long Interspersed Nuclear Element-1 (LINE-1) repeats, makes them responsible for the molecular origin of several diseases. This involves several molecular mechanisms that are presented in this review: insertional mutation, DNA recombination and chromosomal rearrangements, modification of gene expression, as well as alteration of epigenetic regulations. This literature review also presents some of the more recent and/or more classical examples of human diseases in which TEs are involved. Whether through insertion of LINE-1 or Alu elements that cause chromosomal rearrangements, or through epigenetic modifications, TEs are widely implicated in the origin of human cancers. Many other human diseases can have a molecular origin in TE-mediated chromosomal recombination or alteration of gene structure and/or expression. These diseases are very diverse and include hemoglobinopathies, metabolic and neurological diseases, and common diseases. Moreover, TEs can also have an impact on aging. Finally, the exposure of individuals to stresses and environmental contaminants seems to have a non-negligible impact on the epigenetic derepression and mobility of TEs, which can lead to the development of diseases. Thus, improving our knowledge of TEs may lead to new potential diagnostic markers of diseases. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Oncogenes)
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21 pages, 1678 KiB  
Review
Role of the Transcription Factor FOSL1 in Organ Development and Tumorigenesis
by Vladimir V. Sobolev, Asiat Z. Khashukoeva, Olga E. Evina, Natalia A. Geppe, Svetlana N. Chebysheva, Irina M. Korsunskaya, Ekaterina Tchepourina and Alexandre Mezentsev
Int. J. Mol. Sci. 2022, 23(3), 1521; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031521 - 28 Jan 2022
Cited by 27 | Viewed by 3827
Abstract
The transcription factor FOSL1 plays an important role in cell differentiation and tumorigenesis. Primarily, FOSL1 is crucial for the differentiation of several cell lineages, namely adipocytes, chondrocytes, and osteoblasts. In solid tumors, FOSL1 controls the progression of tumor cells through the epithelial–mesenchymal transformation. [...] Read more.
The transcription factor FOSL1 plays an important role in cell differentiation and tumorigenesis. Primarily, FOSL1 is crucial for the differentiation of several cell lineages, namely adipocytes, chondrocytes, and osteoblasts. In solid tumors, FOSL1 controls the progression of tumor cells through the epithelial–mesenchymal transformation. In this review, we summarize the available data on FOSL1 expression, stabilization, and degradation in the cell. We discuss how FOSL1 is integrated into the intracellular signaling mechanisms and provide a comprehensive analysis of FOSL1 influence on gene expression. We also analyze the pathological changes caused by altered Fosl1 expression in genetically modified mice. In addition, we dedicated a separate section of the review to the role of FOSL1 in human cancer. Primarily, we focus on the FOSL1 expression pattern in solid tumors, FOSL1 importance as a prognostic factor, and FOSL1 perspectives as a molecular target for anticancer therapy. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Oncogenes)
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22 pages, 4994 KiB  
Review
Role of Precision Oncology in Type II Endometrial and Prostate Cancers in the African Population: Global Cancer Genomics Disparities
by Rahaba Marima, Rodney Hull, Mandisa Mbeje, Thulo Molefi, Kgomotso Mathabe, Abdulrahman M. Elbagory, Demetra Demetriou and Zodwa Dlamini
Int. J. Mol. Sci. 2022, 23(2), 628; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23020628 - 06 Jan 2022
Cited by 7 | Viewed by 4090
Abstract
Precision oncology can be defined as molecular profiling of tumors to identify targetable alterations. Emerging research reports the high mortality rates associated with type II endometrial cancer in black women and with prostate cancer in men of African ancestry. The lack of adequate [...] Read more.
Precision oncology can be defined as molecular profiling of tumors to identify targetable alterations. Emerging research reports the high mortality rates associated with type II endometrial cancer in black women and with prostate cancer in men of African ancestry. The lack of adequate genetic reference information from the African genome is one of the major obstacles in exploring the benefits of precision oncology in the African context. Whilst external factors such as the geography, environment, health-care access and socio-economic status may contribute greatly towards the disparities observed in type II endometrial and prostate cancers in black populations compared to Caucasians, the contribution of African ancestry to the contribution of genetics to the etiology of these cancers cannot be ignored. Non-coding RNAs (ncRNAs) continue to emerge as important regulators of gene expression and the key molecular pathways involved in tumorigenesis. Particular attention is focused on activated/repressed genes and associated pathways, while the redundant pathways (pathways that have the same outcome or activate the same downstream effectors) are often ignored. However, comprehensive evidence to understand the relationship between type II endometrial cancer, prostate cancer and African ancestry remains poorly understood. The sub-Saharan African (SSA) region has both the highest incidence and mortality of both type II endometrial and prostate cancers. Understanding how the entire transcriptomic landscape of these two reproductive cancers is regulated by ncRNAs in an African cohort may help elucidate the relationship between race and pathological disparities of these two diseases. This review focuses on global disparities in medicine, PCa and ECa. The role of precision oncology in PCa and ECa in the African population will also be discussed. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Oncogenes)
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