Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

5.3K
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...
5.3K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

4.9K
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...
4.9K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

6.1K
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...
6.1K
Anaphase Promoting Complex00:50

Anaphase Promoting Complex

3.5K
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...
3.5K
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

5.7K
Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic...
5.7K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

8.2K
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...
8.2K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Optimization of the Macrocyclic Tetrapeptide [D-Trp]CJ-15,208 to Prevent Stress-Induced Relapse of Cocaine-Seeking Behavior.

Molecules (Basel, Switzerland)·2025
Same author

A Bicyclic Analog of the Linear Peptide Arodyn Is a Potent and Selective Kappa Opioid Receptor Antagonist.

Molecules (Basel, Switzerland)·2024
Same author

Editorial: Plant-based drugs: the potential novel therapeutic intervention against cancer stemness and metastasis.

Frontiers in pharmacology·2023
Same author

Tryptophan Substitution in CJ-15,208 (<i>cyclo</i>[Phe-D-Pro-Phe-Trp]) Introduces δ-Opioid Receptor Antagonism, Preventing Antinociceptive Tolerance and Stress-Induced Reinstatement of Extinguished Cocaine-Conditioned Place Preference.

Pharmaceuticals (Basel, Switzerland)·2023
Same author

Enhancing the Visibility of Women in the ACS Division of Medicinal Chemistry (ACS MEDI).

ACS medicinal chemistry letters·2023
Same author

DAXX drives de novo lipogenesis and contributes to tumorigenesis.

Nature communications·2023

Related Experiment Video

Updated: Feb 27, 2026

MR Molecular Imaging of Prostate Cancer with a Small Molecular CLT1 Peptide Targeted Contrast Agent
06:54

MR Molecular Imaging of Prostate Cancer with a Small Molecular CLT1 Peptide Targeted Contrast Agent

Published on: September 3, 2013

11.8K

Macrocyclic peptides decrease c-Myc protein levels and reduce prostate cancer cell growth.

Archana Mukhopadhyay1,2, Laura E Hanold2, Hamsa Thayele Purayil3

  • 1a Department of Medicinal Chemistry , The University of Kansas , Lawrence , Kansas , USA.

Cancer Biology & Therapy
|July 11, 2017
PubMed
Summary

The macrocyclic peptide [D-Trp]CJ-15,208 effectively reduces c-Myc oncoprotein levels in prostate cancer cells, inhibiting proliferation and inducing apoptosis. This compound shows promise as a novel therapeutic agent for prostate cancer treatment.

Keywords:
CJ-15,208Prostate cancer[D-Trp]CJ-15,208apoptosisc-Myccell cycle arrestmacrocyclic tetrapeptides

More Related Videos

MicroRNA Detection in Prostate Tumors by Quantitative Real-time PCR qPCR
08:30

MicroRNA Detection in Prostate Tumors by Quantitative Real-time PCR qPCR

Published on: May 16, 2012

25.1K
miRNA Expression Analyses in Prostate Cancer Clinical Tissues
11:29

miRNA Expression Analyses in Prostate Cancer Clinical Tissues

Published on: September 8, 2015

11.3K

Related Experiment Videos

Last Updated: Feb 27, 2026

MR Molecular Imaging of Prostate Cancer with a Small Molecular CLT1 Peptide Targeted Contrast Agent
06:54

MR Molecular Imaging of Prostate Cancer with a Small Molecular CLT1 Peptide Targeted Contrast Agent

Published on: September 3, 2013

11.8K
MicroRNA Detection in Prostate Tumors by Quantitative Real-time PCR qPCR
08:30

MicroRNA Detection in Prostate Tumors by Quantitative Real-time PCR qPCR

Published on: May 16, 2012

25.1K
miRNA Expression Analyses in Prostate Cancer Clinical Tissues
11:29

miRNA Expression Analyses in Prostate Cancer Clinical Tissues

Published on: September 8, 2015

11.3K

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • The oncoprotein c-Myc is frequently overexpressed in cancer, making its stability crucial for cancer cell fate.
  • Targeting c-Myc levels presents a promising strategy for developing novel cancer therapeutics.

Purpose of the Study:

  • To investigate the anti-cancer activity of macrocyclic peptides [D-Trp]CJ-15,208 and CJ-15,208.
  • To evaluate the potential of [D-Trp]CJ-15,208 as a therapeutic agent for prostate cancer.

Main Methods:

  • Treatment of prostate cancer cells with [D-Trp]CJ-15,208 and CJ-15,208.
  • Assessment of c-Myc protein levels, cell proliferation (IC50), apoptosis, and cell cycle phase.
  • Investigation of c-Myc's role in sensitivity to [D-Trp]CJ-15,208.
  • Analysis of Protein Phosphatase 2A (PP2A) regulation.

Main Results:

  • [D-Trp]CJ-15,208 significantly reduced c-Myc protein levels and cell proliferation in prostate cancer cell lines (IC50: 2.0–16 µM).
  • [D-Trp]CJ-15,208 induced apoptosis and G2 cell cycle arrest in PC-3 cells.
  • Downregulation of c-Myc decreased sensitivity, while overexpression increased sensitivity to [D-Trp]CJ-15,208.
  • [D-Trp]CJ-15,208 regulated PP2A by decreasing its phosphorylated form, impacting c-Myc stability.

Conclusions:

  • [D-Trp]CJ-15,208 demonstrates potent anti-cancer activity against prostate cancer by targeting c-Myc.
  • The peptide's mechanism involves regulating PP2A, affecting c-Myc stability.
  • [D-Trp]CJ-15,208 is a promising lead compound for developing new prostate cancer treatments.