Related Experiment Video

Updated: Jun 27, 2025

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

1.5K

Metochalcone induces senescence-associated secretory phenotype via JAK2/STAT3 pathway in breast cancer

Jianbo Zhou1,2,3, Feng Wan2,4, Bin Xiao5

  • 1Department of Pharmacology, West China School of Pharmacy, Sichuan University, Chengdu, China.

Oncology Research
|April 30, 2024
PubMed

Insights

Metochalcone (TEC), a chalcone derivative, effectively inhibits breast and lung cancer cell proliferation and tumor growth. It works by inducing senescence-associated secretory phenotype (SASP) through the JAK2/STAT3 pathway, offering potential for new cancer therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Breast and lung cancers are leading global causes of mortality.
  • Chalcones exhibit antitumor activity, but mechanisms of specific analogs like metochalcone (TEC) are unclear.
  • Understanding TEC's molecular targets is crucial for developing novel cancer treatments.

Purpose of the Study:

  • To investigate the molecular mechanisms of 2', 4', 4-trihydroxychalcone (metochalcone; TEC) against breast and lung cancer cells.
  • To elucidate TEC's effects on cell proliferation, cell cycle, migration, and tumor growth.
  • To identify the specific signaling pathways modulated by TEC.

Main Methods:

  • Cell proliferation assays using BT549 (breast) and A549 (lung) cancer cell lines.
  • In vitro cell migration assays and in vivo tumor growth studies.
  • Transcriptomic analysis to identify modulated signaling pathways (JAK2/STAT3, P53).

Main Results:

  • TEC inhibited proliferation of breast and lung cancer cells in a dose-dependent manner.
  • TEC induced S-phase cell cycle arrest, inhibited cell migration, and reduced tumor growth.
  • TEC modulated JAK2/STAT3 and P53 pathways, triggering senescence-associated secretory phenotype (SASP) by repressing JAK2/STAT3.

Conclusions:

  • Metochalcone (TEC) demonstrates significant antitumor effects against breast and lung cancer models.
  • TEC's mechanism involves inducing SASP via the JAK2/STAT3 pathway, suggesting its potential in senescence-based cancer therapy.
  • Chalcone derivatives represent a promising class of compounds for developing novel carcinoma treatments.
Keywords:
Breast cancerJAK2/STAT3Lung cancerMetochalconeSASP

More Related Videos

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence13:59

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

Published on: August 12, 2018

8.1K
SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs07:39

SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs

Published on: June 28, 2019

23.9K

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...
3.8K
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...
8.8K
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...
3.5K
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...
6.3K
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...
5.5K
Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
8.7K