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

PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

3.4K
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...
3.4K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.8K
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
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

6.4K
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...
6.4K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

6.2K
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...
6.2K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

8.7K
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...
8.7K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

5.3K
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...
5.3K

You might also read

Related Articles

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

Sort by
Same author

Nutrient source, temperature, and wetness duration influence fungal growth and conidial germination of <i>Coniella vitis</i>, the main causal agent of grape white rot in China.

Plant disease·2026
Same author

The current status and influencing factors of prophylactic antibacterial drug use in patients with hypertriglyceridemic acute pancreatitis.

Naunyn-Schmiedeberg's archives of pharmacology·2026
Same author

Decoding Fetal Cardiac Trajectories in Gestational Diabetes: Moving Toward Multidimensional Assessment and Precision Monitoring.

Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine·2026
Same author

Enhanced survival in resectable duodenal adenocarcinoma with adjuvant chemotherapy: evidence from a retrospective study.

Frontiers in oncology·2026
Same author

Clinical Serum-Anchored Computational Design Pipeline for a Broad-Spectrum Influenza Multi-Epitope mRNA Vaccine.

Biology·2026
Same author

Highly Efficient Elimination of As(V) and As(III) from Aqueous Media Utilizing Fe-Ti-Mn/Chitosan Composite Xerogel Beads.

Gels (Basel, Switzerland)·2026

Related Experiment Video

Updated: Jun 12, 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

STEAP3 promotes triple-negative breast cancer growth through the FGFR1-mediated activation of PI3K/AKT/mTOR

Lifang Yuan1,2, Yuhan Bao3, Junbao Liu4

  • 1Department of Oncology, Yantai Yuhuangding Hospital, Shandong University, Yantai 264001, China.

Iscience
|June 9, 2025
PubMed
Summary

Six-transmembrane epithelial antigen of prostate 3 (STEAP3) drives aggressive triple-negative breast cancer (TNBC) growth and spread. Targeting STEAP3 may offer a new therapeutic strategy for TNBC patients.

Keywords:
CancerCell biologyMolecular biology

More Related Videos

Studying TGF-&#946; Signaling and TGF-&#946;-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

12.8K
Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NF&#954;B Activity and Breast Cancer Stem Cells
13:38

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells

Published on: January 18, 2017

12.2K

Related Experiment Videos

Last Updated: Jun 12, 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
Studying TGF-&#946; Signaling and TGF-&#946;-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

12.8K
Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NF&#954;B Activity and Breast Cancer Stem Cells
13:38

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells

Published on: January 18, 2017

12.2K

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype with limited targeted therapy options.
  • The role of Six-transmembrane epithelial antigen of prostate 3 (STEAP3) in TNBC remains largely uncharacterized.

Purpose of the Study:

  • To investigate the function and molecular mechanisms of STEAP3 in triple-negative breast cancer progression.
  • To evaluate STEAP3 as a potential therapeutic target for TNBC.

Main Methods:

  • Correlation analysis of STEAP3 expression with proliferation markers in TNBC and non-TNBC.
  • In vitro assays assessing the impact of STEAP3 on cell proliferation, invasion, and metastasis.
  • Mechanistic studies involving FGFR1 stabilization and PI3K/AKT/mTOR pathway activation.
  • In vivo xenograft models to assess tumor growth after STEAP3 knockdown.

Main Results:

  • STEAP3 expression positively correlates with proliferation markers specifically in TNBC.
  • STEAP3 significantly enhances TNBC cell proliferation, invasion, and metastasis in vitro.
  • STEAP3 promotes TNBC progression by stabilizing FGFR1, activating the PI3K/AKT/mTOR pathway.
  • STEAP3 knockdown suppresses tumor growth and proliferation markers in vivo.

Conclusions:

  • STEAP3 is a key regulator of TNBC progression through FGFR1-mediated PI3K/AKT/mTOR signaling.
  • STEAP3 represents a promising therapeutic target for triple-negative breast cancer.