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Related Concept Videos

lncRNA - Long Non-coding RNAs02:39

lncRNA - Long Non-coding RNAs

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In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...
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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...
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Experimental RNAi

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RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
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  1. Home
  3. Characterization Of An Endoplasmic Reticulum Stress-associated Lncrna Prognostic Signature And The Tumor-suppressive Role Of Rp11-295g20.2 Knockdown In Lung Adenocarcinoma.
  1. Home
  3. Characterization Of An Endoplasmic Reticulum Stress-associated Lncrna Prognostic Signature And The Tumor-suppressive Role Of Rp11-295g20.2 Knockdown In Lung Adenocarcinoma.

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RNA Pull-down Procedure to Identify RNA Targets of a Long Non-coding RNA
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Characterization of an endoplasmic reticulum stress-associated lncRNA prognostic signature and the tumor-suppressive

Liying Yu1,2,3, Shuang Zhou4, Wencong Hong4

  • 1Central Laboratory, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, 362000, China. yly20070567@126.com.

Scientific Reports
|May 29, 2024

View abstract on PubMed

Summary
This summary is machine-generated.
Keywords:
Endoplasmic reticulum stressImmunityLung adenocarcinomaPrognosisRP11-295G20.2lncRNA

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This study identifies nine endoplasmic reticulum stress-related long non-coding RNAs (lncRNAs) that predict prognosis in lung adenocarcinoma (LUAD). A risk model using these lncRNAs highlights differences in tumor progression and immunity between high- and low-risk LUAD patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genomics

Background:

  • Endoplasmic reticulum stress (ERS) is crucial in the tumor microenvironment, often triggered by protein misfolding.
  • Long non-coding RNAs (lncRNAs) are implicated in ERS response and lung adenocarcinoma (LUAD) progression, but their specific prognostic roles in LUAD are unclear.

Purpose of the Study:

  • To identify ERS-associated lncRNAs with prognostic value in LUAD.
  • To develop and validate a predictive model for LUAD patient survival based on ERS-related lncRNAs.
  • To investigate the clinical implications and potential therapeutic targeting of these lncRNAs.

Main Methods:

  • Cox and least absolute shrinkage and selection operator (LASSO) regression analyses were used to identify prognostic ERS-related lncRNAs.
  • A risk prediction model was constructed to classify LUAD patients into high-risk (HS) and low-risk (LS) groups.
  • Comprehensive bioinformatic analyses, including functional enrichment and validation in clinical samples, were performed.

    • Main Results:

    • Nine ERS-related lncRNAs (five protective, four risk factors) were identified as independent prognostic indicators.
    • The developed risk model effectively predicted overall survival and stratified LUAD patients.
    • HS patients exhibited advanced-stage tumors, higher mutation burdens, impaired anti-tumor immunity, and reduced drug sensitivity compared to LS patients.
    • Functional analysis linked these lncRNAs to cell migration, death, and immunity.
    • Knockdown of the risk lncRNA RP11-295G20.2 reduced ERS and suppressed LUAD cell proliferation, invasion, and migration.

    Conclusions:

    • A novel ERS-related lncRNA signature serves as a valuable biomarker for prognostic prediction in LUAD.
    • The lncRNA RP11-295G20.2 is a potential therapeutic target for LUAD, as its modulation affects ERS and tumor progression.