Related Experiment Video

Updated: Mar 9, 2026

Real-Time Quantitative Measurement of Tumor Cell Migration and Invasion Following Synthetic mRNA Transfection
11:00

Real-Time Quantitative Measurement of Tumor Cell Migration and Invasion Following Synthetic mRNA Transfection

Published on: June 23, 2023

2.3K

Myc suppresses tumor invasion and cell migration by inhibiting JNK signaling

X Ma1, J Huang1, Y Tian2

  • 1Institute of Intervention Vessel, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Science and Technology, Tongji University, Shanghai, China.

Oncogene
|January 10, 2017
PubMed

Insights

The oncoprotein Myc inhibits tumor invasion and cell migration. Loss of Myc accelerates metastasis, revealing a potential challenge for cancer therapies targeting Myc.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Tumor metastasis is a leading cause of cancer mortality.
  • Drosophila melanogaster serves as a model for studying cancer progression mechanisms.
  • Identifying novel regulators of tumor invasion is crucial for therapeutic development.

Purpose of the Study:

  • To identify novel modulators of tumor invasion using Drosophila.
  • To investigate the role of the oncoprotein Myc in tumor metastasis.
  • To elucidate the molecular mechanisms underlying Myc's function in cell migration.

Main Methods:

  • Genetic screening in Drosophila melanogaster to identify invasion modulators.
  • In vivo analysis of tumor cell migration and invasion.
  • Quantitative analysis of gene transcription, including puc.
  • Validation in human lung adenocarcinoma cell lines.

Main Results:

  • The oncoprotein Myc was identified as a negative regulator of tumor invasion.
  • Loss of Myc expression significantly promotes cell migration in vivo.
  • Myc/Max complex directly upregulates the transcription of puc, an inhibitor of JNK signaling.
  • Human c-Myc suppresses JNK-dependent cell invasion and migration in both Drosophila and human lung cancer cells.

Conclusions:

  • Myc acts as a suppressor of tumor invasion and metastasis by upregulating puc, which inhibits JNK signaling.
  • Therapeutic strategies inhibiting Myc may paradoxically enhance tumor metastasis, posing a challenge for cancer treatment.
  • These findings offer new molecular insights into Myc-mediated cancer progression.

More Related Videos

Tumor Allotransplantation in Drosophila melanogaster with a Programmable Auto-Nanoliter Injector05:06

Tumor Allotransplantation in Drosophila melanogaster with a Programmable Auto-Nanoliter Injector

Published on: February 2, 2021

2.8K
Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion09:23

Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion

Published on: April 2, 2020

6.9K

Related Concept Videos

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...
5.3K
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

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...
5.8K
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...
5.0K
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...
8.9K
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...
7.6K
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...
13.5K