Related Experiment Video

Updated: Oct 28, 2025

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
11:42

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells

Published on: April 7, 2017

9.6K

Association of RDM1 with osteosarcoma progression via cell cycle and MEK/ERK signalling pathway regulation

Jun Sheng1, Kun Liu2, Dawei Sun1

  • 1Department of Orthopedics, Xinqiao Hospital, Army Medical University, Chongqing, China.

Journal of Cellular and Molecular Medicine
|July 15, 2021
PubMed

Insights

RAD52 motif-containing 1 (RDM1) promotes osteosarcoma (OS) progression by driving cell cycle and MEK/ERK signaling. Inhibiting RDM1 offers a potential therapeutic strategy for osteosarcoma treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • RAD52 motif-containing 1 (RDM1) is implicated in DNA repair and cancer development.
  • RDM1's role in osteosarcoma (OS) progression and its underlying mechanisms are not well understood.

Purpose of the Study:

  • To investigate the role of RDM1 in osteosarcoma progression.
  • To elucidate the molecular mechanisms by which RDM1 influences OS.

Main Methods:

  • Quantitative analysis of RDM1 expression in OS cells versus osteoblasts.
  • In vitro experiments involving RDM1 knockdown and overexpression in OS cells.
  • In vivo studies using a xenograft mouse model.
  • Western blot analysis to assess MEK/ERK pathway protein levels.

Main Results:

  • RDM1 expression is significantly higher in osteosarcoma cells compared to normal osteoblasts.
  • RDM1 knockdown inhibits OS cell proliferation, induces apoptosis, and causes G1 cell cycle arrest.
  • RDM1 overexpression reverses these effects.
  • RDM1 silencing reduces tumor growth in vivo.
  • RDM1 upregulates the protein levels of MEK1/2 and ERK1/2.

Conclusions:

  • RDM1 functions as an oncogene in osteosarcoma.
  • RDM1 promotes OS progression by facilitating G1 to S phase cell cycle transition and activating the MEK/ERK signaling pathway.
  • RDM1 represents a potential therapeutic target for osteosarcoma treatment.
Keywords:
MEK/ERK signalling pathwayOsteosarcomaRDM1cell cycle

More Related Videos

A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate07:31

A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate

Published on: May 3, 2021

3.9K
Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

379

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...
4.0K
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...
4.3K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
6.7K
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...
4.8K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
7.2K
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...
5.1K