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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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Inheritance of Chromatin Structures03:17

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Epigenetics is the study of inherited changes in a cell's phenotype without changing the DNA sequences. It provides a form of memory for the differential gene expression pattern to maintain cell lineage, position-effect variegation, dosage compensation, and maintenance of chromatin structures such as telomeres and centromeres. For example, the structure and location of the centromere on chromosomes are epigenetically inherited. Its functionality is not dictated or ensured by the underlying...
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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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Abnormal Proliferation02:23

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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Related Experiment Video

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In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
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Long Non-Coding RNA DUXAP10 Promotes Tumorigenesis and Metastasis in Anaplastic Thyroid Cancer.

Nicole R DeSouza1, Michelle Carnazza1, Tara Jarboe1

  • 1Department of Pathology, Microbiology & Immunology, New York Medical College, Valhalla, NY 10595, USA.

Cancers
|December 11, 2025
PubMed
Summary

Long non-coding RNA DUXAP10 drives anaplastic thyroid cancer (ATC) progression. Inhibiting DUXAP10 reduced tumor growth and metastasis, identifying it as a potential therapeutic target for this lethal cancer.

Keywords:
RNA therapeuticscancerlong non-coding RNAsmiRNAsregulatory non-coding variantsribodiagnosticstargeted therapy

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Spontaneous Murine Model of Anaplastic Thyroid Cancer
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Area of Science:

  • Molecular Biology
  • Genomics
  • Cancer Research

Background:

  • Long non-coding RNAs (lncRNAs) regulate gene expression and impact cancer development.
  • Anaplastic thyroid cancer (ATC) is an aggressive and lethal malignancy with poorly understood molecular mechanisms.
  • Understanding lncRNA dysregulation in ATC is crucial for identifying new therapeutic targets.

Purpose of the Study:

  • To investigate the role of lncRNA Double Homeobox A Pseudogene 10 (DUXAP10) in anaplastic thyroid cancer.
  • To determine if DUXAP10 is a potential therapeutic target for ATC.

Main Methods:

  • Analysis of patient genomic datasets to identify upregulated lncRNAs in ATC.
  • CRISPR-interference (CRISPRi) technology to transcriptionally repress DUXAP10 expression in ATC cell lines.
  • In vitro and in vivo experiments to assess the functional impact of DUXAP10 on ATC phenotypes.

Main Results:

  • DUXAP10 was found to be significantly upregulated in ATC compared to normal thyroid tissue.
  • Repression of DUXAP10 using CRISPRi markedly reduced ATC cell proliferation, viability, clonogenicity, invasion, and migration.
  • DUXAP10 inhibition also suppressed in vivo tumor growth and metastasis in preclinical models.

Conclusions:

  • DUXAP10 plays a critical role in promoting the aggressive phenotypes of anaplastic thyroid cancer.
  • DUXAP10 serves as a potential prognostic marker for ATC.
  • DUXAP10 represents a promising therapeutic target for combating ATC progression.