Related Experiment Video

Updated: Jun 8, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

Jun amino-terminal kinase 1 activation promotes cell survival in ErbB2-positive breast cancer

Ji Seung Han1, David L Crowe

  • 1University of Illinois Cancer Center, Chicago, IL 60612, USA.

Anticancer Research
|October 15, 2010
PubMed
Abstract

Insights

JNK1 kinase promotes survival in Her2/neu-positive breast cancer. Inhibiting JNK1 induces apoptosis and reduces tumor growth in preclinical models, offering a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Signaling

Background:

  • Her2/neu overexpression is critical in human breast cancer.
  • Key survival pathways involve mitogen- and stress-activated protein kinases (MAPKs) like ERK, JNK, and p38.

Purpose of the Study:

  • To investigate the role of MAPK signaling in Her2/neu-driven breast cancer.
  • To determine if JNK1 activation is specific to Her2/neu-positive cancers.
  • To evaluate JNK1 inhibition as a therapeutic strategy.

Main Methods:

  • Examined MAPK protein expression in mouse and human cancer tissues.
  • Inhibited MAPK expression using genetic and pharmacologic approaches in human breast cancer cell lines.
  • Assessed the impact of MAPK inhibition on tumor formation in a preclinical model.

Main Results:

  • High levels of activated JNK1 were observed in MMTV-neu mouse tumors and Her2/neu-overexpressing human breast cancer cell lines.
  • JNK1 inhibition led to specific apoptosis induction in these cell lines.
  • A JNK1 inhibitor increased tumor latency and decreased tumor growth in MMTV-neu mice by inducing apoptosis.

Conclusions:

  • JNK1 is preferentially activated in Her2/neu-positive breast cancer.
  • JNK1 plays a crucial role in promoting cell survival in this cancer type.
  • Targeting JNK1 represents a potential therapeutic avenue for Her2/neu-positive breast cancer.

Related Concept Videos

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...
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...
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 rapamycin-insensitive companion...
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...
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...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

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...