Related Experiment Video

Updated: Jul 28, 2025

Author Spotlight: A Selective Luciferase-Based Assay for Monitoring ATG4B 27 Activity in Cells
09:51

Author Spotlight: A Selective Luciferase-Based Assay for Monitoring ATG4B 27 Activity in Cells

Published on: June 30, 2023

921

CircHIPK3 negatively regulates autophagy by blocking VCP binding to the Beclin 1 complex in bladder cancer

Chong Wang1,2,3, Tiantian Liu1,2, Jiawei Wang2

  • 1Department of Urology, The Fifth Affiliated Hospital Sun Yat-Sen University, Zhuhai, 519000, Guangdong, People's Republic of China.

Discover Oncology
|June 3, 2023
PubMed

Insights

Circular RNA HIPK3 (circHIPK3) is downregulated in bladder cancer, promoting cell proliferation and autophagy. It inhibits VCP-mediated autophagy, suggesting a role in bladder cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Circular RNA HIPK3 (circHIPK3) is implicated in various cancers.
  • The specific role of circHIPK3 in regulating autophagy in bladder cancer remains largely unknown.
  • Autophagy is a critical cellular process involved in cell survival and death.

Purpose of the Study:

  • To elucidate the mechanism by which circHIPK3 regulates autophagy in bladder cancer cells.
  • To investigate the interaction of circHIPK3 with binding proteins involved in autophagy.
  • To determine the potential regulatory pathway of circHIPK3 in bladder cancer.

Main Methods:

  • Quantitative analysis of circHIPK3 and autophagy-related proteins in bladder cancer tissues and cells.
  • Assessment of bladder cancer cell proliferation under varying circHIPK3 expression levels.
  • Investigation of circHIPK3's effect on the VCP/Beclin 1 interaction and autophagy.
  • Analysis of VCP's role in stabilizing Beclin 1 and regulating autophagy via ataxin-3.

Main Results:

  • CircHIPK3 levels were significantly lower in bladder cancer compared to normal tissues, with corresponding upregulation of autophagy proteins.
  • Downregulation of circHIPK3 promoted bladder cancer cell proliferation, while its overexpression inhibited proliferation.
  • Overexpression of circHIPK3 suppressed autophagy and disrupted the VCP/Beclin 1 interaction.
  • VCP was found to stabilize Beclin 1 and promote autophagy by downregulating ataxin-3.

Conclusions:

  • CircHIPK3 plays a significant role in bladder cancer progression.
  • CircHIPK3 inhibits VCP-mediated autophagy in bladder cancer cells.
  • circHIPK3 may represent a potential therapeutic target for bladder cancer treatment.
Keywords:
AutophagyBladder cancerCircular RNARNA-binding proteins (RBPs)VCP

More Related Videos

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells09:10

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

Published on: October 28, 2019

7.3K
Evaluating Autophagy Levels in Two Different Pancreatic Cell Models Using LC3 Immunofluorescence08:07

Evaluating Autophagy Levels in Two Different Pancreatic Cell Models Using LC3 Immunofluorescence

Published on: April 28, 2023

1.6K

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.8K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
6.6K
Anaphase Promoting Complex00:50

Anaphase Promoting Complex

The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
2.9K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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.
The mTOR pathway or the...
3.8K
Autophagy01:27

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
4.4K
Abnormal Proliferation02:23

Abnormal Proliferation

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...
4.6K