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

Drugs that Stabilize Microtubules01:15

Drugs that Stabilize Microtubules

Microtubules are dynamic structures that undergo cycles of catastrophe and rescue. The microtubules play a central role in cell division by forming the spindle apparatus for segregating the chromosomes. This makes them ideal targets for regulating dividing cells in tumors and malignant cancer cells. Microtubule stabilizing drugs help stabilize the microtubule formation and promote its polymerization. Paclitaxel was the first microtubule stabilizing agent used as anticancer drug in chemotherapy...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...

You might also read

Related Articles

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

Sort by
Same author

Starving leukemia: nicotinamide phosphoribosyltransferase-dependent nicotinamide adenine dinucleotide salvage links metabolic vulnerability to therapeutic sensitivity in acute myeloid leukemia.

Translational cancer research·2026
Same author

Targeting "undruggable" cancer proteins: pharmacological challenges and emerging strategies.

Translational cancer research·2026
Same author

Synthesis of <i>N</i>‑Substituted Acenaphtho[1,2‑<i>b</i>]pyrroles and Dibenzo[<i>e,g</i>]indoles with Promising Antileukemic Activity from Morita-Baylis-Hillman Adducts.

ACS omega·2026
Same author

Does coordinated targeting of metabolism and autophagy, modulated by microtubule dynamics, influence therapeutic vulnerability to eribulin in glioblastoma?

Translational cancer research·2026
Same author

Molecular and Antiangiogenic Effects of Paclitaxel-Loaded Nanoparticles: Influence of the Nanocarrier Type.

Molecular pharmaceutics·2026
Same author

Repositioning HDAC Inhibitors for Glioma Treatment: Synthesis and Biological Evaluation.

ACS omega·2026

Related Experiment Video

Updated: Jul 12, 2026

An Ex Vivo Brain Slice Model to Study and Target Breast Cancer Brain Metastatic Tumor Growth
10:38

An Ex Vivo Brain Slice Model to Study and Target Breast Cancer Brain Metastatic Tumor Growth

Published on: September 22, 2021

SIVA1 Knockdown Drives Aggressive Phenotypes in Triple-Negative Breast Cancer Cells while Enhancing Paclitaxel

Natália Sudan Parducci1, Bruna Oliveira de Almeida1, Anali Del Milagro Bernabe Garnique1

  • 1Department of Pharmacology, Institute of Biomedical Sciences, Universidade de São Paulo, São Paulo CEP 05508-900, Brazil.

ACS Omega
|July 10, 2026
PubMed
Summary

The study reveals SIVA1 protein overexpression in breast cancer promotes tumor growth and drug resistance. Inhibiting SIVA1 increases aggressiveness but enhances sensitivity to paclitaxel, offering new therapeutic strategies.

More Related Videos

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel
08:29

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel

Published on: May 14, 2018

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
06:00

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

Published on: May 14, 2016

Related Experiment Videos

Last Updated: Jul 12, 2026

An Ex Vivo Brain Slice Model to Study and Target Breast Cancer Brain Metastatic Tumor Growth
10:38

An Ex Vivo Brain Slice Model to Study and Target Breast Cancer Brain Metastatic Tumor Growth

Published on: September 22, 2021

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel
08:29

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel

Published on: May 14, 2018

Through the Looking Glass: Time-lapse Microscopy and Longitudinal Tracking of Single Cells to Study Anti-cancer Therapeutics
06:00

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

Published on: May 14, 2016

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • SIVA1 is a multifunctional protein implicated in tumor progression.
  • Its specific role in breast cancer, despite frequent overexpression, is not well-defined.
  • Understanding SIVA1's molecular network is crucial for breast cancer research.

Purpose of the Study:

  • To elucidate the cellular mechanisms regulated by SIVA1 in breast cancer.
  • To characterize the molecular network associated with SIVA1.
  • To investigate the functional impact of SIVA1 on breast cancer cell behavior and drug sensitivity.

Main Methods:

  • Integrated in silico analyses and in vitro assays using breast cancer cell lines.
  • Assessment of cell proliferation, migration, invasion, and drug sensitivity in 2D and 3D models.
  • Molecular analyses of DNA damage, apoptosis, cytoskeletal regulators, ubiquitination, and p53 signaling.

Main Results:

  • SIVA1 overexpression is linked to pathways involved in protein secretion, DNA repair, and oxidative stress.
  • SIVA1 knockdown increased proliferation, migration, and invasion, but enhanced sensitivity to paclitaxel.
  • Knockdown led to increased DNA damage markers (γ-H2AX), apoptosis (cleaved PARP1), and altered p53 and Stathmin 1 signaling.

Conclusions:

  • SIVA1 is a key regulator of proliferation and cytoskeletal dynamics in breast cancer.
  • Inhibiting SIVA1 promotes a more aggressive phenotype but increases taxane sensitivity.
  • Findings suggest SIVA1's potential role in patient stratification and therapeutic decision-making for breast cancer treatment.