Related Experiment Video

Updated: Oct 12, 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

1.1K

ARID3A regulates autophagy related gene BECN1 expression and inhibits proliferation of osteosarcoma cells

Cuneyd Parlayan1, Yunus Sahin2, Zekiye Altan2

  • 1Department of Biostatistics and Medical Informatics, School of Medicine, Bahcesehir University, Istanbul, Turkey.

Biochemical and Biophysical Research Communications
|November 21, 2021
PubMed

Insights

ARID3A acts as a tumor suppressor in osteosarcoma (OS) by upregulating BECN1 expression. Silencing ARID3A promotes cancer cell proliferation, highlighting its therapeutic potential.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Osteosarcoma (OS) is a common primary bone cancer with poorly understood molecular mechanisms.
  • Identifying key regulators of OS progression is crucial for developing novel therapeutic strategies.
  • ARID3A, a DNA-binding protein, is implicated in OS pathogenesis and interacts with E2F1, a regulator of autophagy gene BECN1.

Purpose of the Study:

  • To investigate the role of ARID3A in regulating BECN1 expression in osteosarcoma cells.
  • To explore the functional impact of ARID3A on osteosarcoma cell proliferation and colony formation.

Main Methods:

  • Gene expression analysis of ARID3A, BECN1, and E2F1 in U-2 OS cells using qPCR.
  • Validation of gene expression and prognostic value using GEO and Kaplan-Meier plotter databases.
  • Experimental manipulation of ARID3A levels (overexpression and silencing) to assess effects on BECN1 expression and cell behavior.

Main Results:

  • BECN1 expression showed a positive correlation with ARID3A and a negative correlation with E2F1 in OS.
  • ARID3A overexpression led to increased BECN1 levels, while ARID3A silencing decreased BECN1 expression.
  • ARID3A silencing enhanced U-2 OS cell proliferation and colony formation, whereas ARID3A overexpression suppressed these processes.

Conclusions:

  • ARID3A functions as a tumor suppressor in osteosarcoma.
  • ARID3A influences osteosarcoma progression, at least partly, through the regulation of BECN1 expression.
Keywords:
ARID3AAutophagyBECN1Beclin1E2F1Osteosarcoma

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

7.4K
Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

1.8K

Related Concept Videos

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...
3.9K
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...
4.7K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
4.1K
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,...
4.8K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
2.3K
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...
5.0K