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Gene Expression Regulation of Long Non-coding RNAs in Cancer

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A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (15 September 2023) | Viewed by 8470

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Special Issue Editors

Dr. Crystal N. Marconett

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Guest Editor

Department of Surgery, Keck School of Medicine, University of Southern California, Los Angeles, CA 90089, USA
Interests: long non-coding RNA; lung cancer; DNA damage repair; alveolar epithelial cell biology
Special Issues, Collections and Topics in MDPI journals

Dr. Linlin Guo

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Guest Editor

Department of Obstetrics and Gynaecology, The Ohio State University Wexner Medical Center, Columbus, OH, USA
Interests: cancer; therapy; signaling pathway; HER; EGF; Wnt; notch; TGF-β; mTOR; PD-1/PD-L1
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue will encompass recent research on the form and function of long non-coding RNAs (lncRNAs) that play a causal role in the etiology of cancer. LncRNAs will be the central focus of this Special Issue, including but not limited to their transcriptional regulation; miRNA targetting; partnering interactions in protein complexes; and mechanisms in the initiation, promotion, and progression of lung cancer. This Special Issue will also encompass the utility of lncRNAs as biomarkers of cancer and the effect that specific lncRNAs play on patient outcomes and response to current therapies.

Dr. Crystal N. Marconett
Dr. Linlin Guo
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. Cancers is an international peer-reviewed open access semimonthly 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 2900 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

lncRNAs in cancer
mechanisms of lncRNA function
regulatory RNA function
scaffolding RNAs
lncRNA signaling components

Published Papers (4 papers)

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Research

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17 pages, 4189 KiB

Open AccessArticle

LncRNA SNHG1 Facilitates Tumor Proliferation and Represses Apoptosis by Regulating PPARγ Ubiquitination in Bladder Cancer

by Hongzhou Cai, Haifei Xu, Hongcheng Lu, Weizhang Xu, Haofeng Liu, Xinwei Wang, Guoren Zhou and Xuejian Yang

Cancers 2022, 14(19), 4740; https://doi.org/10.3390/cancers14194740 - 28 Sep 2022

Cited by 7 | Viewed by 1565

Abstract

Background: Long noncoding RNAs regulate various biological effects in the progression of cancers. We found that the expression of SNHG1 was significantly up-regulated in bladder cancer after analyzing data obtained from TCGA and GEO. However, the potential role of SNHG1 remains to be investigated in bladder cancer. It was validated that SNHG1 was overexpressed in bladder cancer tissues detected by qRT-PCR and FISH, which was also associated with poor clinical outcome. Additionally, SNHG1 was verified to facilitate tumor proliferation and repress apoptosis in vitro and in vivo. Results: SNHG1 could act as a competitive endogenous RNA and decrease the expression of murine double minute 2 (MDM2) by sponging microRNA-9-3p. Furthermore, MDM2 induced ubiquitination and degradation of PPARγ that contributed to the development of bladder cancer. Conclusions: the study elucidated that SNHG1 played an important role in bladder cancer and provided a potential therapeutic target for bladder cancer. Full article

(This article belongs to the Special Issue Gene Expression Regulation of Long Non-coding RNAs in Cancer)

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18 pages, 27277 KiB

Open AccessArticle

HSF1 Stimulates Glutamine Transport by Super-Enhancer-Driven lncRNA LINC00857 in Colorectal Cancer

by Qi Shen, Rui Wang, Xinling Liu, Ping Song, Mingzhu Zheng, Xiaomin Ren, Jingang Ma, Zhong Lu and Jiaqiu Li

Cancers 2022, 14(16), 3855; https://doi.org/10.3390/cancers14163855 - 9 Aug 2022

Cited by 12 | Viewed by 2337

Abstract

Super enhancers are critical for the gene transcription responsible for cell fate by interacting with transcription factors. However, the relevance of HSF1 to super enhancers in tumors remains obscure. We profiled H3K27ac enrichment by chromatin immunoprecipitation sequencing. HSF1-mediated lncRNAs were identified by lncRNA microarray. The characteristics of LINC00857 were explored by in vitro and in vivo assays. The mechanism was studied via chromatin immunoprecipitation, RNA immunoprecipitation, and HSF1/ANXA11 knockout mice. We found that super enhancers occupied multiple gene loci in colorectal cancer. We screened out an HSF1-mediated super enhancer, lncRNA-LINC00857, which exerts its characteristics in promoting cell growth via regulating glutamine metabolism. Notably, HSF1 could stimulate the super-enhancer activity of LINC00857 by the enrichment of acetyltransferase P300 to its gene loci, contributing to LINC00857 transcription. In turn, nuclear LINC00857 cooperated with HSF1 to promote ANXA11 transcription, which modulated SLC1A5/ASCT2 protein expression by binding competitively to miR-122-5p. The knockout of ANXA11 attenuated colorectal cancer formation in vivo. Collectively, we shed light on a closely cooperative machinery between HSF1 and super enhancers. HSF1 could stimulate acetyltransferase P300-mediated super-enhancer activity to facilitate LINC00857 expression, contributing to SLC1A5-mediated glutamine transport. Targeting the HSF1/LINC00857/ANXA11 axis may provide a valuable therapeutic strategy against colorectal cancer. Full article

(This article belongs to the Special Issue Gene Expression Regulation of Long Non-coding RNAs in Cancer)

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21 pages, 6412 KiB

Open AccessArticle

HOXA11-AS1 Promotes PD-L1-Mediated Immune Escape and Metastasis of Hypopharyngeal Carcinoma by Facilitating PTBP1 and FOSL1 Association

by Zheng Zhou, Qian Liu, Gehou Zhang, Diab Mohammed, Sani Amadou, Guolin Tan and Xiaowei Zhang

Cancers 2022, 14(15), 3694; https://doi.org/10.3390/cancers14153694 - 29 Jul 2022

Cited by 5 | Viewed by 1992

Abstract

Background: The metastatic characteristics of hypopharyngeal squamous cell carcinoma (HSCC) lead to many diagnostic and therapeutic challenges, while functional long non-coding RNAs (lncRNAs) can provide effective strategies for its diagnosis and treatment. Methods: RT-qPCR, Western blot, immunohistochemistry, and an immunofluorescence assay were used to detect the related gene expression. Flow cytometry was used to measure the percentage of CD8⁺ and CD4⁺ T cells. CCK-8 and transwell assays were performed to analyze the role of HOXA11-AS1. The targeted relationship of the FOSL1/PD-L1 promoter was measured by ChIP and dual-luciferase reporter assays. RNA pulldown and RIP assays were used to measure the interaction between HOXA11-AS1, FOSL1, and PTBP1. A tumor xenograft study was used to analyze HOXA11-AS1 function in vivo. Results: HOXA11-AS1, PD-L1, and FOSL1 were upregulated in HSCC, and HOXA11-AS1 positively correlated with PD-L1. HOXA11-AS1 knockdown upregulated CD8⁺ T cells through an increase in IFN-γ concentration while decreasing the proliferation, migration, and invasion of HSCC cells. FOSL1 bound the PD-L1 promoter, increasing gene expression. HOXA11-AS1 enhanced the stability of FOSL1 mRNA by binding to PTBP1. HOXA11-AS1 or PTBP1 overexpression increased FOSL1 and PD-L1 expression. PD-L1 knockdown arrested the inhibiting function of HOXA11-AS1 overexpression on CD8⁺ T cell content. HOXA11-AS1 knockdown inhibited immune escape and metastasis through PD-L1 regulation by downregulating FOSL1 in vivo. Conclusion: HOXA11-AS1 promoted PD-L1 expression by upregulating FOSL1 levels through PTBP1, thereby facilitating immune escape, proliferation, and metastasis of HSCC cells. Full article

(This article belongs to the Special Issue Gene Expression Regulation of Long Non-coding RNAs in Cancer)

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Review

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27 pages, 1202 KiB

Open AccessReview

The Talented LncRNAs: Meshing into Transcriptional Regulatory Networks in Cancer

by Dana Segal and Josée Dostie

Cancers 2023, 15(13), 3433; https://doi.org/10.3390/cancers15133433 - 30 Jun 2023

Cited by 5 | Viewed by 1975

Abstract

As a group of diseases characterized by uncontrollable cell growth, cancer is highly multifaceted in how it overrides checkpoints controlling proliferation. Amongst the regulators of these checkpoints, long non-coding RNAs (lncRNAs) can have key roles in why natural biological processes go haywire. LncRNAs represent a large class of regulatory transcripts that can localize anywhere in cells. They were found to affect gene expression on many levels from transcription to mRNA translation and even protein stability. LncRNA participation in such control mechanisms can depend on cell context, with given transcripts sometimes acting as oncogenes or tumor suppressors. Importantly, the tissue-specificity and low expression levels of lncRNAs make them attractive therapeutic targets or biomarkers. Here, we review the various cellular processes affected by lncRNAs and outline molecular strategies they use to control gene expression, particularly in cancer and in relation to transcription factors. Full article

(This article belongs to the Special Issue Gene Expression Regulation of Long Non-coding RNAs in Cancer)

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