Related Experiment Video

Updated: Sep 23, 2025

A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate
07:31

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

Published on: May 3, 2021

3.8K

β-Escin inhibits the proliferation of osteosarcoma cells via blocking the PI3K/Akt pathway

Minyu Zhu1, Jinwei Ying1, Chaowei Lin1

  • 1Department of Spine Surgery, The First Affiliated Hospital of Wenzhou Medical University Nanbaixiang Street, Ouhai District Wenzhou 325000 Zhejiang China 907173102@qq.com +8613587688135 +8613587688135.

RSC Advances
|May 13, 2022
PubMed

Insights

Beta-escin demonstrates significant anticancer activity against human osteosarcoma (OS) cells both in vitro and in vivo. This compound inhibits proliferation and induces apoptosis, partly by inactivating the PI3K/Akt signaling pathway.

Area of Science:

  • Pharmacology
  • Oncology
  • Biochemistry

Background:

  • Beta-escin is known for its anticancer properties against various cancer types.
  • The specific effects of beta-escin on human osteosarcoma (OS) remain largely unexplored.

Purpose of the Study:

  • To investigate the efficacy of beta-escin against human osteosarcoma (OS) both in vitro and in vivo.
  • To elucidate the underlying molecular mechanisms of beta-escin's anti-OS effects.

Main Methods:

  • Cell proliferation assays using multiple OS cell lines (MG-63, OS732, U-2OS, HOS, SAOS-2).
  • In vivo studies using an OS xenograft model.
  • Apoptosis assays, Western blotting for key proteins (caspases, Bax, Bcl-2, PI3K/Akt/mTOR pathway).
  • Synergy studies with conventional chemotherapeutic agents (cisplatin, MTX, Dox, Ifos).

Main Results:

  • Beta-escin exhibited dose- and time-dependent inhibition of OS cell proliferation.
  • Beta-escin demonstrated significant anti-proliferative and pro-apoptotic effects in vivo.
  • Beta-escin synergized with cisplatin, methotrexate, doxorubicin, and ifosfamide to inhibit OS cell proliferation.
  • Beta-escin induced apoptosis, activated caspases, and modulated Bax/Bcl-2 expression.
  • Beta-escin treatment reduced the expression of p-PI3K, p-Akt, and p-mTOR, and Akt activation reversed its anti-proliferative effects.

Conclusions:

  • Beta-escin effectively inhibits osteosarcoma proliferation both in vitro and in vivo.
  • The anti-proliferative mechanism of beta-escin involves the inactivation of the PI3K/Akt signaling pathway.
  • Beta-escin holds potential as a therapeutic agent for osteosarcoma, possibly in combination therapy.

More Related Videos

Intratibial Osteosarcoma Cell Injection to Generate Orthotopic Osteosarcoma and Lung Metastasis Mouse Models04:25

Intratibial Osteosarcoma Cell Injection to Generate Orthotopic Osteosarcoma and Lung Metastasis Mouse Models

Published on: October 28, 2021

10.0K
Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma08:07

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma

Published on: April 12, 2019

7.3K

Related Concept Videos

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
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
9.3K
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
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