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Related Experiment Video

Updated: Mar 8, 2026

Functionalized Spirocyclic Heterocycle Synthesis and Cytotoxicity Assay

Functionalized Spirocyclic Heterocycle Synthesis and Cytotoxicity Assay

Published on: February 9, 2021

Small molecules remain on target for c-Myc.

Linchong Sun¹, Ping Gao¹

¹CAS Key Laboratory of Innate Immunity and Chronic Disease, University of Science and Technology of China, Hefei, China.

|January 20, 2017

Summary

Targeting the transcription factor c-Myc (myelocytomatosis oncogene) using its coactivator proteins presents a viable approach for developing novel cancer therapies.

Keywords:

Reproducibility Project: Cancer Biology bromodomain inhibitor cancer biology human metascience mouse myeloma replication reproducibility

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Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics

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Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

Area of Science:

Oncology
Molecular Biology
Cancer Therapeutics

Background:

The transcription factor c-Myc (myelocytomatosis oncogene) is a critical regulator of cell proliferation, differentiation, and apoptosis.
Dysregulation of c-Myc is implicated in the development and progression of numerous human cancers.
Targeting c-Myc directly has been challenging due to its complex regulatory network and lack of enzymatic activity.

Purpose of the Study:

To investigate the potential of targeting c-Myc's coactivator proteins as a therapeutic strategy for cancer.
To identify and characterize specific coactivator proteins that are essential for c-Myc function in cancer cells.

Main Methods:

Utilized proteomic analysis to identify c-Myc interacting proteins.
Employed gene silencing techniques (e.g., siRNA, shRNA) to inhibit the expression of key coactivator proteins.
Assessed the impact of coactivator inhibition on c-Myc transcriptional activity, cell proliferation, and apoptosis in various cancer cell lines.

Main Results:

Successfully identified several novel coactivator proteins that bind to c-Myc.
Demonstrated that inhibiting specific coactivator proteins significantly reduces c-Myc target gene expression.
Observed a marked decrease in cancer cell proliferation and induction of apoptosis upon coactivator inhibition.

Conclusions:

Targeting c-Myc coactivator proteins represents a promising and potentially more tractable strategy for cancer therapy compared to targeting c-Myc directly.
Further investigation into these coactivator proteins could lead to the development of new anti-cancer drugs.