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Non-coding RNAs in Tumor Development and Angiogenesis

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 December 2023) | Viewed by 9461

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Special Issue Editors

Prof. Dr. Binghua Jiang

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Guest Editor

Department of Pathology, Anatomy and Cell Biolog, Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA
Interests: cancer development; cancer therapeutic resistance; carcinogenesis; angiogenesis
Special Issues, Collections and Topics in MDPI journals

Dr. Ling-Zhi Liu

E-Mail Website
Guest Editor

Department of Medical Oncology, Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA 19107, USA
Interests: carcinogenesis; angiogenesis; cancer resistance
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Non-coding RNAs have been demonstrated to be important in cancer development, angiogenesis, biomarkers, and therapeutic resistance. micro-RNAs (miRNAs) are the first class of non-coding RNAs discovered in cancer development to have a therapeutic effect, and are the most extensively investigated ncRNAs in regulation of cancer initiation, development, angiogenesis, and therapeutic resistance. long-ncRNAs (lncRNAs) represent the largest class of non-coding RNAs, with more than 55,000 genes in the human genome, and lncRNAs may regulate gene expression through their interactions with proteins, miRNAs, DNA, and mRNAs. Other ncRNAs may also play important roles in some forms of cancer development. NcRNAs may regulate multiple molecular and cellular processes, such as RNA stability, protein translation, post-transcriptional regulations, DNA methylation, chromatin remodeling, and signal transduction.

This Special Issue will focus on recent research to understand the networks and mechanisms of ncRNAs, especially miRNAs and LncRNAs, that are key regulators of cancer initiation, carcinogenesis, development, angiogenesis, cellular programs, and therapeutic resistance. Gaining improved understanding of the complex networks of ncRNAs and underlining molecular mechanisms will provide new opportunities to identify new biomarkers and to design new options for cancer treatments in the future.

Prof. Dr. Binghua Jiang
Dr. Ling-Zhi Liu
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

LnRNA
miRNA
cancer
carcinogenesis
angiogenesis
drug resistance
epigenetic regulation
DNA and RNA methylation

Published Papers (4 papers)

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Research

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19 pages, 10078 KiB

Open AccessArticle

Developing Folate-Conjugated miR-34a Therapeutic for Prostate Cancer: Challenges and Promises

by Wen (Jess) Li, Yunfei Wang, Xiaozhuo Liu, Shan Wu, Moyi Wang, Steven G. Turowski, Joseph A. Spernyak, Amanda Tracz, Ahmed M. Abdelaal, Kasireddy Sudarshan, Igor Puzanov, Gurkamal Chatta, Andrea L. Kasinski and Dean G. Tang

Int. J. Mol. Sci. 2024, 25(4), 2123; https://doi.org/10.3390/ijms25042123 - 9 Feb 2024

Cited by 2 | Viewed by 1129

Abstract

Prostate cancer (PCa) remains a common cancer with high mortality in men due to its heterogeneity and the emergence of drug resistance. A critical factor contributing to its lethality is the presence of prostate cancer stem cells (PCSCs), which can self-renew, long-term propagate tumors, and mediate treatment resistance. MicroRNA-34a (miR-34a) has shown promise as an anti-PCSC therapeutic by targeting critical molecules involved in cancer stem cell (CSC) survival and functions. Despite extensive efforts, the development of miR-34a therapeutics still faces challenges, including non-specific delivery and delivery-associated toxicity. One emerging delivery approach is ligand-mediated conjugation, aiming to achieve specific delivery of miR-34a to cancer cells, thereby enhancing efficacy while minimizing toxicity. Folate-conjugated miR-34a (folate–miR-34a) has demonstrated promising anti-tumor efficacy in breast and lung cancers by targeting folate receptor α (FOLR1). Here, we first show that miR-34a, a TP53 transcriptional target, is reduced in PCa that harbors TP53 loss or mutations and that miR-34a mimic, when transfected into PCa cells, downregulated multiple miR-34a targets and inhibited cell growth. When exploring the therapeutic potential of folate–miR-34a, we found that folate–miR-34a exhibited impressive inhibitory effects on breast, ovarian, and cervical cancer cells but showed minimal effects on and targeted delivery to PCa cells due to a lack of appreciable expression of FOLR1 in PCa cells. Folate–miR-34a also did not display any apparent effect on PCa cells expressing prostate-specific membrane antigen (PMSA) despite the reported folate’s binding capability to PSMA. These results highlight challenges in the specific delivery of folate–miR-34a to PCa due to a lack of target (receptor) expression. Our study offers novel insights into the challenges and promises within the field and casts light on the development of ligand-conjugated miR-34a therapeutics for PCa. Full article

(This article belongs to the Special Issue Non-coding RNAs in Tumor Development and Angiogenesis)

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16 pages, 3676 KiB

Open AccessArticle

Transcriptional Regulation of Siglec-15 by ETS-1 and ETS-2 in Hepatocellular Carcinoma Cells

by Kaiqin Sheng, Yuecheng Wu, Hanbin Lin, Menghan Fang, Chaorong Xue, Xu Lin and Xinjian Lin

Int. J. Mol. Sci. 2023, 24(1), 792; https://doi.org/10.3390/ijms24010792 - 2 Jan 2023

Viewed by 1999

Abstract

Sialic acid-binding immunoglobulin-like lectin 15 (Siglec-15) has been identified as a crucial immune suppressor in human cancers, comparable to programmed cell death 1 ligand (PD-L1). However, the regulatory mechanisms underlying its transcriptional upregulation in human cancers remain largely unknown. Here, we show that the transcription factors ETS-1 and ETS-2 bound to the Siglec-15 promoter to enhance transcription and expression of Siglec-15 in hepatocellular carcinoma (HCC) cells and that transforming growth factor β-1 (TGF-β1) upregulated the expression of ETS-1 and ETS-2 and facilitated the binding of ETS-1 and ETS-2 to the Siglec-15 promoter. We further demonstrate that TGF-β1 activated the Ras/C-Raf/MEK/ERK1/2 signaling pathway, leading to phosphorylation of ETS-1 and ETS-2, which consequently upregulates the transcription and expression of Siglec-15. Our study defines a detailed molecular profile of how Siglec-15 is transcriptionally regulated which may offer significant opportunity for therapeutic intervention on HCC immunotherapy. Full article

(This article belongs to the Special Issue Non-coding RNAs in Tumor Development and Angiogenesis)

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Review

Jump to: Research

42 pages, 2191 KiB

Open AccessReview

Connection between Radiation-Regulating Functions of Natural Products and miRNAs Targeting Radiomodulation and Exosome Biogenesis

by Jen-Yang Tang, Ya-Ting Chuang, Jun-Ping Shiau, Ching-Yu Yen, Fang-Rong Chang, Yi-Hong Tsai, Ammad Ahmad Farooqi and Hsueh-Wei Chang

Int. J. Mol. Sci. 2023, 24(15), 12449; https://doi.org/10.3390/ijms241512449 - 4 Aug 2023

Cited by 2 | Viewed by 1757

Abstract

Exosomes are cell-derived membranous structures primarily involved in the delivery of the payload to the recipient cells, and they play central roles in carcinogenesis and metastasis. Radiotherapy is a common cancer treatment that occasionally generates exosomal miRNA-associated modulation to regulate the therapeutic anticancer function and side effects. Combining radiotherapy and natural products may modulate the radioprotective and radiosensitizing responses of non-cancer and cancer cells, but there is a knowledge gap regarding the connection of this combined treatment with exosomal miRNAs and their downstream targets for radiation and exosome biogenesis. This review focuses on radioprotective natural products in terms of their impacts on exosomal miRNAs to target radiation-modulating and exosome biogenesis (secretion and assembly) genes. Several natural products have individually demonstrated radioprotective and miRNA-modulating effects. However, the impact of natural-product-modulated miRNAs on radiation response and exosome biogenesis remains unclear. In this review, by searching through PubMed/Google Scholar, available reports on potential functions that show radioprotection for non-cancer tissues and radiosensitization for cancer among these natural-product-modulated miRNAs were assessed. Next, by accessing the miRNA database (miRDB), the predicted targets of the radiation- and exosome biogenesis-modulating genes from the Gene Ontology database (MGI) were retrieved bioinformatically based on these miRNAs. Moreover, the target-centric analysis showed that several natural products share the same miRNAs and targets to regulate radiation response and exosome biogenesis. As a result, the miRNA–radiomodulation (radioprotection and radiosensitization)–exosome biogenesis axis in regard to natural-product-mediated radiotherapeutic effects is well organized. This review focuses on natural products and their regulating effects on miRNAs to assess the potential impacts of radiomodulation and exosome biogenesis for both the radiosensitization of cancer cells and the radioprotection of non-cancer cells. Full article

(This article belongs to the Special Issue Non-coding RNAs in Tumor Development and Angiogenesis)

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17 pages, 1130 KiB

Open AccessReview

ROS and miRNA Dysregulation in Ovarian Cancer Development, Angiogenesis and Therapeutic Resistance

by David C. Stieg, Yifang Wang, Ling-Zhi Liu and Bing-Hua Jiang

Int. J. Mol. Sci. 2022, 23(12), 6702; https://doi.org/10.3390/ijms23126702 - 16 Jun 2022

Cited by 15 | Viewed by 3840

Abstract

The diverse repertoires of cellular mechanisms that progress certain cancer types are being uncovered by recent research and leading to more effective treatment options. Ovarian cancer (OC) is among the most difficult cancers to treat. OC has limited treatment options, especially for patients diagnosed with late-stage OC. The dysregulation of miRNAs in OC plays a significant role in tumorigenesis through the alteration of a multitude of molecular processes. The development of OC can also be due to the utilization of endogenously derived reactive oxygen species (ROS) by activating signaling pathways such as PI3K/AKT and MAPK. Both miRNAs and ROS are involved in regulating OC angiogenesis through mediating multiple angiogenic factors such as hypoxia-induced factor (HIF-1) and vascular endothelial growth factor (VEGF). The NAPDH oxidase subunit NOX4 plays an important role in inducing endogenous ROS production in OC. This review will discuss several important miRNAs, NOX4, and ROS, which contribute to therapeutic resistance in OC, highlighting the effective therapeutic potential of OC through these mechanisms. Full article

(This article belongs to the Special Issue Non-coding RNAs in Tumor Development and Angiogenesis)

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