Related Experiment Video

Updated: Oct 19, 2025

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

8.8K

Akt Phosphorylation Orchestrates T11TS Mediated Cell Cycle Arrest in Glioma Cells

Sagar Acharya1, Sirshendu Chatterjee2, Suhnrita Chaudhuri3

  • 1Department of Zoology, Vidyasagar University, Paschim Medinipur, Midnapore, India.

Cancer Investigation
|September 27, 2021
PubMed

Insights

The novel glycopeptide T11TS halts glioma growth by affecting key cell signaling pathways. This research details how T11TS induces glioma cell death through specific molecular interactions.

Area of Science:

  • Neuro-oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Gliomas are aggressive brain tumors with limited treatment options.
  • The tumor microenvironment significantly influences glioma progression and treatment response.

Purpose of the Study:

  • To investigate the mechanism by which the novel anti-neoplastic glycopeptide T11TS induces glioma cell arrest and death.
  • To explore the correlation between T11TS-mediated alterations in the glioma microenvironment and tumor suppression.

Main Methods:

  • Utilized flow cytometry, immunoblotting, ELISA, and co-immunoprecipitation to analyze glioma cell responses.
  • Examined the phosphorylation status of key proteins involved in cell survival and apoptosis pathways.

Main Results:

  • T11TS treatment led to a decrease in Akt phosphorylation.
  • Observed attenuation of p21 phosphorylation and dissociation of p-Akt-Mdm2 and p-Akt-BAD complexes.
  • Identified T11TS's influence on Akt signaling pathways, specifically Akt>p21 and Akt>Mdm2>p53.

Conclusions:

  • T11TS effectively retards glioma growth in vitro and in vivo.
  • The anti-cancer effects of T11TS are mediated through the modulation of critical cell signaling pathways, promoting glioma cell death.
  • This study provides key insights into the molecular mechanisms underlying T11TS-induced glioma cell arrest and death.
Keywords:
AktGliomaT11TSapoptosiscell cycle arrest

More Related Videos

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells12:52

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells

Published on: November 28, 2015

16.0K
Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice10:13

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice

Published on: August 12, 2014

13.6K

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...
4.2K
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
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
DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
9.5K
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
36.6K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
6.7K