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Functional Analysis and Therapeutic Targets of Long Non-Coding RNAs
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Functional Analysis and Therapeutic Targets of Long Non-Coding RNAs

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

Deadline for manuscript submissions: 20 March 2025 | Viewed by 2544

Special Issue Editor

Dr. Hidenori Tani

E-Mail Website
Guest Editor
Department of Health Pharmacy, Yokohama University of Pharmacy, 601 Matano, Totsuka, Yokohama, Japan
Interests: lncRNA function; RNA stability; RNA drug discovery; liquid–liquid phase separation (LLPS); stress response; RNA splicing; machine learning; RNA–protein interaction network
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Long non-coding RNAs (lncRNAs) have emerged as crucial regulators of gene expression and cellular processes, with their dysregulation being implicated in various human diseases. Consequently, lncRNAs have gained significant attention as promising therapeutic targets. The aim of this Special Issue is to provide a comprehensive overview of the latest advances in the functional analysis and therapeutic targeting of lncRNAs, with a particular emphasis on the development of novel lncRNA-based therapies.

We welcome original research articles and review manuscripts addressing the following two topics: (a) lncRNA-targeted therapeutics: This Special Issue will highlight the development of novel therapeutic strategies targeting lncRNAs, including approaches that modulate lncRNA function, stability, and localization. (b) lncRNA-based therapeutic modalities: Submissions exploring a wide range of therapeutic modalities for targeting lncRNAs, such as antisense oligonucleotides, small interfering RNAs (siRNAs), CRISPR/Cas9 gene editing, and small-molecule modulators, are highly encouraged. It is believed that this Special Issue will serve as a valuable resource for researchers and clinicians working in the field of lncRNA biology and therapeutics.

Dr. Hidenori Tani
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

  • lncRNAs
  • gene expression
  • cellular processes
  • disease dysregulation
  • therapeutic targets
  • functional analysis
  • lncRNA therapeutics
  • lncRNA modulation
  • stability
  • localization

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Published Papers (2 papers)

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Research

18 pages, 22923 KiB  
Article
Activation of the G Protein-Coupled Bile Acid Receptor TGR5 Modulates the HCP5/miR-139-5p/DDIT4 Axis to Antagonize Cervical Cancer Progression
by Jia Su, Yiqi Zhao, Wei-Dong Chen and Yan-Dong Wang
Int. J. Mol. Sci. 2024, 25(16), 8932; https://doi.org/10.3390/ijms25168932 - 16 Aug 2024
Viewed by 937
Abstract
A growing body of evidence indicates that the G protein-coupled bile acid receptor, TGR5, plays a critical role in multiple physiological processes ranging from metabolic disorders to cancers. However, the biological functions of TGR5 in cervical cancer (CC) have not been elucidated. Here, [...] Read more.
A growing body of evidence indicates that the G protein-coupled bile acid receptor, TGR5, plays a critical role in multiple physiological processes ranging from metabolic disorders to cancers. However, the biological functions of TGR5 in cervical cancer (CC) have not been elucidated. Here, using TGR5 knockout mice, we found that a deficiency of TGR5 leads to greater sensitivity to the progression of cervical inflammation. Activation of TGR5 by its specific ligands significantly attenuated the malignant behavior of CC cells. In addition, we found that TGR5 can negatively modulate the expression of lncRNA HCP5 by blocking its transcription activation when mediated by p65. HCP5 was highly expressed in CC tissues, which was positively correlated with the poor prognosis of CC patients. HCP5 knockdown notably restrained CC cell proliferation, colony formation, and migration in vitro, and inhibited tumor growth in vivo. Furthermore, HCP5 can function as the molecular sponge for miR-139-5p to upregulate DNA damage-induced transcript 4 (DDIT4) in CC cells. Murine xenograft studies demonstrated that TGR5 suppressed the tumor formation of CC cells and downregulated HCP5 and DDIT4 while increasing miR-139-5p in the xenografts. Taken together, these findings, for the first time, indicate that TGR5 inhibits CC progression by regulating the HCP5/miR-139-5p/DDIT4 axis, suggesting that it may represent a novel and potent target for CC treatment. Full article
(This article belongs to the Special Issue Functional Analysis and Therapeutic Targets of Long Non-Coding RNAs)
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10 pages, 1578 KiB  
Communication
Identification of Two Long Noncoding RNAs, Kcnq1ot1 and Rmst, as Biomarkers in Chronic Liver Diseases in Mice
by Shinya Yokoyama, Hisanori Muto, Takashi Honda, Yoichi Kurokawa, Hirotaka Ogawa, Riku Nakajima, Hiroki Kawashima and Hidenori Tani
Int. J. Mol. Sci. 2024, 25(16), 8927; https://doi.org/10.3390/ijms25168927 - 16 Aug 2024
Viewed by 1001
Abstract
This study investigates novel short-lived long noncoding RNAs (lncRNAs) in mice with altered expression in metabolic dysfunction-associated steatotic liver (MASH) and liver fibrosis. LncRNAs share similarities with mRNAs in their transcription by RNA polymerase II, possession of a 5′ cap structure, and presence [...] Read more.
This study investigates novel short-lived long noncoding RNAs (lncRNAs) in mice with altered expression in metabolic dysfunction-associated steatotic liver (MASH) and liver fibrosis. LncRNAs share similarities with mRNAs in their transcription by RNA polymerase II, possession of a 5′ cap structure, and presence of a polyA tail. We identified two lncRNAs, Kcnq1ot1 and Rmst, significantly decreased in both conditions. These lncRNAs showed dramatic expression changes in MASH livers induced by Western diets and CCl4, and in fibrotic livers induced by CCl4 alone. The decrease was more pronounced in liver fibrosis, suggesting their potential as biomarkers for disease progression. Our findings are consistent across different fibrosis models, indicating a crucial role for these lncRNAs in MASH and liver fibrosis in mice. With MASH becoming a global health issue and its progression to fibrosis associated with hepatocarcinogenesis and poor prognosis, understanding the underlying mechanisms is critical. This research contributes to elucidating lncRNA functions in murine liver diseases and provides a foundation for developing novel therapeutic strategies targeting lncRNAs in MASH and liver fibrosis, offering new avenues for potential therapeutic interventions. Full article
(This article belongs to the Special Issue Functional Analysis and Therapeutic Targets of Long Non-Coding RNAs)
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