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The Significance of Transcription Factors, miRNAs, and lncRNAs in Anticancer Drug Development

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 2755

Special Issue Editors


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Guest Editor
1. Department of Biology, Zanvyl Krieger School of Arts and Sciences, Johns Hopkins University, Baltimore, MD 21218-2685, USA
2. Fellow, National Academy of Inventors, Tampa, FL 33612, USA
3. Academician, Academia Sinica, 128 Academia Road, Section 2, Nankang, Taipei 11529, Taiwan
Interests: chromatin structure and function; tetra-O-methyl nordihydroguaiaretic acid (M4N, terameprocol); oncogenic development in humans; chemotherapeutic drug treatments; viral replication; gene functions
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Co-Guest Editor
Department of Biology, Johns Hopkins University, 3400 N. Charles Street, Baltimore, MD 21218-2685, USA
Interests: anticancer drug; combination drug treatment; transcription factor; gene regulation; alternative splicing; cancer metabolism; mitochondria; apoptosis and hypoxia

Special Issue Information

Dear Colleagues,

Recent progress in systems biology has shown that several specific factors are participants of a network that function as master regulators of cancer. These factors are usually transcription factors, microRNAs (miRNAs), and long non-coding RNAs (lncRNAs) in control of the expression of various genes which play important roles in the regulation of cancer development. This suggests that there may be a way to induce unfavorable effects on cancer development and progression by modulating the activity and/or expression of these specific factors. In this Special Issue, we will focus on studies that investigate the roles and mechanisms of transcription factors, miRNAs, and lncRNAs in the regulation of the expression of cancer-related genes and/or proteins, and explore the search for potential drugs that cause adverse effects on cancer by modulating the activity of these specific factors and thus manipulating the activity and/or expression of various cancer-related genes and/or proteins. In other words, this Special Issue is about the effort to discover potentially effective anticancer drugs by targeting transcription factors, miRNAs, and lncRNAs which function as master regulators of cancer.

Prof. Dr. Ru Chih C. Huang
Dr. Kotohiko Kimura
Guest Editors

Manuscript Submission Information

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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. Current Issues in Molecular Biology 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 2200 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

  • transcription factors
  • microRNAs (miRNAs)
  • long non-coding RNAs (lncRNAs)
  • anticancer drugs
  • cancer
  • coactivators

Published Papers (5 papers)

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Research

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24 pages, 2833 KiB  
Article
Dysregulation of Transposon Transcription Profiles in Cancer Cells Resembles That of Embryonic Stem Cells
by Anna I. Solovyeva, Roman V. Afanasev, Marina A. Popova and Natella I. Enukashvily
Curr. Issues Mol. Biol. 2024, 46(8), 8576-8599; https://doi.org/10.3390/cimb46080505 - 5 Aug 2024
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Abstract
Transposable elements (TEs) comprise a substantial portion of the mammalian genome, with potential implications for both embryonic development and cancer. This study aimed to characterize the expression profiles of TEs in embryonic stem cells (ESCs), cancer cell lines, tumor tissues, and the tumor [...] Read more.
Transposable elements (TEs) comprise a substantial portion of the mammalian genome, with potential implications for both embryonic development and cancer. This study aimed to characterize the expression profiles of TEs in embryonic stem cells (ESCs), cancer cell lines, tumor tissues, and the tumor microenvironment (TME). We observed similarities in TE expression profiles between cancer cells and ESCs, suggesting potential parallels in regulatory mechanisms. Notably, four TE RNAs (HERVH, LTR7, HERV-Fc1, HERV-Fc2) exhibited significant downregulation across cancer cell lines and tumor tissues compared to ESCs, highlighting potential roles in pluripotency regulation. The strong up-regulation of the latter two TEs (HERV-Fc1, HERV-Fc2) in ESCs has not been previously demonstrated and may be a first indication of their role in the regulation of pluripotency. Conversely, tandemly repeated sequences (MSR1, CER, ALR) showed up-regulation in cancer contexts. Moreover, a difference in TE expression was observed between the TME and the tumor bulk transcriptome, with distinct dysregulated TE profiles. Some TME-specific TEs were absent in normal tissues, predominantly belonging to LTR and L1 retrotransposon families. These findings not only shed light on the regulatory roles of TEs in both embryonic development and cancer but also suggest novel targets for anti-cancer therapy. Understanding the interplay between cancer cells and the TME at the TE level may pave the way for further research into therapeutic interventions. Full article
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20 pages, 1449 KiB  
Article
Secondary Analysis of Human Bulk RNA-Seq Dataset Suggests Potential Mechanisms for Letrozole Resistance in Estrogen-Positive (ER+) Breast Cancer
by Lincoln Sutherland, Jacob Lang, Norberto Gonzalez-Juarbe and Brett E. Pickett
Curr. Issues Mol. Biol. 2024, 46(7), 7114-7133; https://doi.org/10.3390/cimb46070424 - 6 Jul 2024
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Abstract
Estrogen receptor-positive (ER+) breast cancer is common among postmenopausal women and is frequently treated with Letrozole, which inhibits aromatase from synthesizing estrogen from androgens. Decreased estrogen slows the growth of tumors and can be an effective treatment. The increase in Letrozole resistance poses [...] Read more.
Estrogen receptor-positive (ER+) breast cancer is common among postmenopausal women and is frequently treated with Letrozole, which inhibits aromatase from synthesizing estrogen from androgens. Decreased estrogen slows the growth of tumors and can be an effective treatment. The increase in Letrozole resistance poses a unique problem for patients. To better understand the underlying molecular mechanism(s) of Letrozole resistance, we reanalyzed transcriptomic data by comparing individuals who responded to Letrozole therapy (responders) to those who were resistant to treatment (non-responders). We identified SOX11 and S100A9 as two significant differentially expressed genes (DEGs) between these patient cohorts, with “PLK1 signaling events” being the most significant signaling pathway. We also identified PRDX4 and E2F8 gene products as being the top mechanistic transcriptional markers for ER+ treatment resistance. Many of the significant DEGs that we identified play a known role in ER+ breast cancer or other types of cancer, which partially validate our results. Several of the gene products we identified are novel in the context of ER+ breast cancer. Many of the genes that we identified warrant further research to elucidate the more specific molecular mechanisms of Letrozole resistance in this patient population and could potentially be used as prognostic markers with further wet lab validation. We anticipate that these findings could contribute to improved detection and therapeutic outcomes in aromatase-resistant ER+ breast cancer patients. Full article
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21 pages, 5275 KiB  
Article
Expression and Functional Analysis of Immuno-Micro-RNAs mir-146a and mir-326 in Colorectal Cancer
by Ovidiu Farc, Liviuta Budisan, Florin Zaharie, Roman Țăulean, Dan Vălean, Elena Talvan, Ioana Berindan Neagoe, Oana Zănoagă, Cornelia Braicu and Victor Cristea
Curr. Issues Mol. Biol. 2024, 46(7), 7065-7085; https://doi.org/10.3390/cimb46070421 - 5 Jul 2024
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Abstract
Micro-RNAs (miRNAs) are non-coding RNAs with importance in the development of cancer. They are involved in both tumor development and immune processes in tumors. The present study aims to characterize the behavior of two miRNAs, the proinflammatory miR-326-5p and the anti-inflammatory miR-146a-5p, in [...] Read more.
Micro-RNAs (miRNAs) are non-coding RNAs with importance in the development of cancer. They are involved in both tumor development and immune processes in tumors. The present study aims to characterize the behavior of two miRNAs, the proinflammatory miR-326-5p and the anti-inflammatory miR-146a-5p, in colorectal cancer (CRC), to decipher the mechanisms that regulate their expression, and to study potential applications. Tissue levels of miR-326-5p and miR-146a-5p were determined by qrt-PCR (real-time quantitative reverse transcription polymerase chain reaction) in 45 patients with colorectal cancer in tumoral and normal adjacent tissue. Subsequent bioinformatic analysis was performed to characterize the transcriptional networks that control the expression of the two miRNAs. The biomarker potential of miRNAs was assessed. The expression of miR-325-5p and miR-146a-5p was decreased in tumors compared to normal tissue. The two miRNAs are regulated through a transcriptional network, which originates in the inflammatory and proliferative pathways and regulates a set of cellular functions related to immunity, proliferation, and differentiation. The miRNAs coordinate distinct modules in the network. There is good biomarker potential of miR-326 with an AUC (Area under the curve) of 0.827, 0.911 sensitivity (Sn), and 0.689 specificity (Sp), and of the combination miR-326-miR-146a, with an AUC of 0.845, Sn of 0.75, and Sp of 0.89. The miRNAs are downregulated in the tumor tissue. They are regulated by a transcriptional network in which they coordinate distinct modules. The structure of the network highlights possible therapeutic approaches. MiR-326 and the combination of the two miRNAs may serve as biomarkers in CRC. Full article
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Review

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17 pages, 891 KiB  
Review
MicroRNAs Associated with IgLON Cell Adhesion Molecule Expression
by Marco Salluzzo, Clara Vianello, Francesca Flotta, Roberto Rimondini and Lucia Carboni
Curr. Issues Mol. Biol. 2024, 46(7), 7702-7718; https://doi.org/10.3390/cimb46070456 - 19 Jul 2024
Viewed by 462
Abstract
The IgLON family of cell adhesion molecules consists of five members (LSAMP, OPCML, neurotrimin, NEGR1, and IgLON5) discovered as supporters of neuronal development, axon growth and guidance, and synapse formation and maintenance. Tumour suppression properties have recently been emerging based on antiproliferative effects [...] Read more.
The IgLON family of cell adhesion molecules consists of five members (LSAMP, OPCML, neurotrimin, NEGR1, and IgLON5) discovered as supporters of neuronal development, axon growth and guidance, and synapse formation and maintenance. Tumour suppression properties have recently been emerging based on antiproliferative effects through the modulation of oncogenic pathways. Available evidence endorses a role for non-coding RNAs or microRNAs as relevant controllers of IgLON molecule expression that can impact their critical physiological and pathological roles. Current findings support a function for long non-coding RNAs and microRNAs in the modulation of LSAMP expression in cell senescence, cancer biogenesis, addiction, and pulmonary hypertension. For OPCML, data point to a role for several microRNAs in the control of tumorigenesis. MicroRNAs were detected in neurotrimin-mediated functions in cancer biogenesis and in Schwann cell responses to peripheral nerve injury. For NEGR1, studies have mainly investigated microRNA involvement in neuronal responses to ischaemic injury, although data also exist about tumorigenesis and endothelial cell dysfunction. For IgLON5, information is only available about microRNA involved in myocardial infarction. In conclusion, despite much information being still missing and further research needed, the emerging picture favours a model in which non-coding RNAs exert a crucial role in modulating IgLON expression, ultimately affecting their important physiological functions. Full article
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11 pages, 1098 KiB  
Review
Mechanism of DAPK1 for Regulating Cancer Stem Cells in Thyroid Cancer
by Mi-Hyeon You
Curr. Issues Mol. Biol. 2024, 46(7), 7086-7096; https://doi.org/10.3390/cimb46070422 - 5 Jul 2024
Viewed by 436
Abstract
Death-associated protein kinase 1 (DAPK1) is a calcium/calmodulin (Ca2+/CaM)-dependent serine/threonine (Ser/Thr) protein kinase and is characteristically downregulated in metastatic cancer. Several studies showed that DAPK1 is involved in both the early and late stages of cancer. DAPK1 downregulation is elaborately controlled [...] Read more.
Death-associated protein kinase 1 (DAPK1) is a calcium/calmodulin (Ca2+/CaM)-dependent serine/threonine (Ser/Thr) protein kinase and is characteristically downregulated in metastatic cancer. Several studies showed that DAPK1 is involved in both the early and late stages of cancer. DAPK1 downregulation is elaborately controlled by epigenetic, transcriptional, posttranscriptional, and posttranslational processes. DAPK1 is known to regulate not only cancer cells but also stromal cells. Recent studies showed that DAPK1 was involved not only in tumor suppression but also in epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) formation in colon and thyroid cancers. CSCs are major factors in determining cancer aggressiveness in cancer metastasis and treatment prognosis by influencing EMT. However, the molecular mechanism involved in the regulation of cancer cells by DAPK1 remains unclear. In particular, little is known about the existence of CSCs and how they are regulated in papillary thyroid carcinoma (PTC) among thyroid cancers. In this review, we describe the molecular mechanism of CSC regulation by DAPK1 in PTC progression. Full article
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