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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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Cancer Stem Cells and Tumor Maintenance02:40

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Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
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Non-LTR Retrotransposons03:18

Non-LTR Retrotransposons

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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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piRNA - Piwi-interacting RNAs02:57

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PIWI-interacting RNAs, or piRNAs, are the most abundant short non-coding RNAs. More than 20,000 genes have been found in humans that code for piRNAs while only 2000 genes have been found for miRNAs. piRNAs can act at the transcriptional and post-transcriptional levels and have a vital role in silencing transposable elements present in germ cells. They are also involved in epigenetic silencing and activation. Previously, they were thought to function only in germ cells but new evidence suggests...
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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
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Long Noncoding RNAs Preserve Pancreatic Cancer Identity and Resist Cell Fate Conversion.

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    Isolation of Stem Cells from Human Pancreatic Cancer Xenografts
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    Area of Science:

    • Cancer Biology
    • Epigenetics
    • Molecular Oncology

    Background:

    • Pancreatic ductal adenocarcinoma (PDAC) exhibits transcriptional plasticity and rigidity, resisting therapy due to persistent malignant transcriptional memory.
    • Epigenetic barriers prevent reprogramming of PDAC cells, even with Yamanaka factors (OCT4, SOX2, KLF4, MYC; OSKM), preserving their resistant identity.
    • The role of long noncoding RNAs (lncRNAs) in enforcing cancer-specific transcriptional memory in PDAC remains largely unexplored.

    Purpose of the Study:

    • To identify and characterize PDAC-enriched lncRNAs that enforce malignant transcriptional memory and confer therapy resistance.
    • To investigate the potential of targeting these lncRNAs to overcome PDAC reprogramming resistance and reduce tumorigenicity.

    Main Methods:

    • Utilized CRISPR interference screens to identify PDAC-specific lncRNAs.
    • Assessed the impact of lncRNA depletion on PDAC reprogramming, malignant gene expression, and in vivo tumorigenicity.
    • Analyzed the association of specific lncRNAs (ATXN7L3-AS1, AC079921.2) with PDAC variants, cell states, and reprogramming resistance.

    Main Results:

    • Identified several PDAC-enriched lncRNAs that, upon depletion, suppress malignant programs, enhance OSKM-mediated reprogramming, and reduce tumor growth.
    • ATXN7L3-AS1 and AC079921.2 were identified as potent lncRNAs, minimally expressed in normal pancreas but upregulated in PDAC.
    • ATXN7L3-AS1 is linked to mitotic progression and pathogenic variants, potentially ensuring malignant program inheritance, while AC079921.2 promotes a mesenchymal-like, invasive state resistant to reprogramming.

    Conclusions:

    • Discovered a novel role for cancer-associated lncRNAs as critical regulators of transcriptional memory in PDAC.
    • These lncRNAs act as gatekeepers of malignant identity, contributing to therapy resistance.
    • Targeting these lncRNAs offers a therapeutic strategy to reset epigenetic states, erase cancer cell memory, and re-sensitize PDAC to therapies.