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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 the pre-miRNA...
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As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
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  1. Home
  2. Research Domains
  3. Biomedical And Clinical Sciences
  4. Oncology And Carcinogenesis
  5. Predictive And Prognostic Markers
  6. Lncrna Slncr1 Facilitates Angiogenesis And Tumor Growth In Melanoma Via Dnmt1-mediated Epigenetically Silencing Spry2.
  1. Home
  2. Research Domains
  3. Biomedical And Clinical Sciences
  4. Oncology And Carcinogenesis
  5. Predictive And Prognostic Markers
  6. Lncrna Slncr1 Facilitates Angiogenesis And Tumor Growth In Melanoma Via Dnmt1-mediated Epigenetically Silencing Spry2.

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LncRNA SLNCR1 facilitates angiogenesis and tumor growth in melanoma via DNMT1-mediated epigenetically silencing SPRY2.

Ke Li1,2, Lijun Wu3, Jingting Jiang1

  • 1Department of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Jiangsu Engineering Research Center for Tumor Immunotherapy, Institute of Cell Therapy, Soochow University, Changzhou, Jiangsu, P. R. China.

Skin Research and Technology : Official Journal of International Society for Bioengineering and the Skin (ISBS) [And] International Society for Digital Imaging of Skin (ISDIS) [And] International Society for Skin Imaging (ISSI)
|September 19, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Long non-coding RNA SLNCR1 promotes melanoma growth and metastasis by suppressing SPRY2 expression via DNMT1-mediated methylation. Targeting SLNCR1 offers a potential therapeutic strategy for melanoma treatment.

Keywords:
DNMT1SPRY2angiogenesislncRNA SLNCR1

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Melanoma malignancy stems from invasiveness, vascularization, and rapid metastasis.
  • Long non-coding RNA SLNCR1 is linked to aggressive tumors, but its role in melanoma angiogenesis is unclear.

Purpose of the Study:

  • To investigate the role of SLNCR1 in melanoma growth, metastasis, and angiogenesis.
  • To elucidate the molecular mechanism by which SLNCR1 influences melanoma progression.

Main Methods:

  • SLNCR1 expression analysis in melanoma tissues and cell lines.
  • In vitro assays (CCK-8, flow cytometry, Western blot) to assess proliferation, migration, and angiogenesis.
  • In vivo xenograft model in nude mice to evaluate tumor growth.
  • ChIP, RIP, and Western blot assays to determine the interaction between SLNCR1, DNMT1, and SPRY2.
melanoma

Main Results:

  • SLNCR1 was significantly upregulated in melanoma tissues and cells.
  • Silencing SLNCR1 reduced melanoma cell proliferation, migration, and HUVEC angiogenesis.
  • SLNCR1 loss inhibited tumor growth and metastasis in vivo.
  • SLNCR1 was found to suppress SPRY2 expression by enhancing DNMT1-mediated promoter methylation.

Conclusions:

  • SLNCR1 acts as an oncogene in melanoma by promoting angiogenesis and tumor growth.
  • SLNCR1 interacts with DNMT1 to epigenetically silence SPRY2, contributing to melanoma progression.
  • SLNCR1 represents a potential therapeutic target for melanoma treatment.