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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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Abnormal Proliferation

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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 Nucleolus02:55

The Nucleolus

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The nucleolus is the most prominent substructure of the nucleus. When it was first discovered, it was considered to be an isolated organelle that forms fibrils and granules. In 1931, the relationship between the nucleolus and chromosomes was first described by Heitz. He observed that the appearance and size of nucleolus varies depending on the stage of the cell cycle. He also noticed constricted regions on different chromosomes clustered together at definite cell cycle stages. These regions,...
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Cancer Cell Migration through Invadopodia01:35

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Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However,...
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Adaptive Mechanisms in Cancer Cells

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Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
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Related Experiment Video

Updated: Apr 29, 2026

Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
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Fusobacterium nucleatum Promotes Bladder Cancer Development Through lncRNA IDH1-AS1-Mediated Autophagy.

JunJie Hu1, BiYan Li2, XiaoYuan Xu1

  • 1Department of Urology, Lanxi People's Hospital, Lanxi, Zhejiang, 321100, China.

Archivum Immunologiae Et Therapiae Experimentalis
|April 27, 2026
PubMed
Summary

The long noncoding RNA IDH1-AS1 promotes bladder cancer growth and proliferation. IDH1-AS1 may serve as a novel biomarker and therapeutic target for bladder cancer.

Keywords:
AutophagyBladder cancerFusobacterium nucleatumlncRNA IDH1-AS1

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Bladder cancer is a common malignancy with high recurrence rates.
  • Long noncoding RNAs (lncRNAs) are increasingly recognized for their roles in cancer progression.
  • Identifying novel molecular targets is crucial for advancing bladder cancer diagnosis and therapy.

Purpose of the Study:

  • To investigate the role of the lncRNA IDH1-AS1 in bladder cancer.
  • To assess the impact of IDH1-AS1 on tumor growth, cell proliferation, and autophagy.
  • To evaluate IDH1-AS1 as a potential biomarker and therapeutic target.

Main Methods:

  • Utilized in vivo (nude mice model) and in vitro models to study IDH1-AS1.
  • Assessed tumor growth, cell proliferation (EDU assay), and autophagy-related protein expression (Western Blot).
  • Quantified IDH1-AS1 gene expression using quantitative polymerase chain reaction (qPCR).

Main Results:

  • IDH1-AS1 overexpression significantly increased tumor volume, weight, and cell proliferation.
  • IDH1-AS1 knockdown significantly decreased tumor size and cell proliferation.
  • IDH1-AS1 modulated autophagy proteins (Beclin1, LC3, P62), suggesting a role in regulating autophagy.

Conclusions:

  • IDH1-AS1 promotes tumor growth and cell proliferation in bladder cancer.
  • IDH1-AS1 may exert its effects by regulating autophagy-related proteins.
  • IDH1-AS1 represents a potential novel biomarker and therapeutic target for bladder cancer treatment.