Related Experiment Video

Updated: May 13, 2026

Quantifying Antibody-Dependent Cellular Cytotoxicity in a Tumor Spheroid Model: Application for Drug Discovery
13:19

Quantifying Antibody-Dependent Cellular Cytotoxicity in a Tumor Spheroid Model: Application for Drug Discovery

Published on: April 26, 2024

Sunitinib reverse multidrug resistance in gastric cancer cells by modulating Stat3 and inhibiting P-gp function

Ye Zhang1, Qiong Wang

  • 1Tumour Therapy Department with Western Medicine & Traditional Chinese Medicine, Wuxi No. 4 People's Hospital, Wuxi Hospital of Oncology, The Fourth Affiliated Hospital of Soochow University, No. 200, Huihe Road, Wuxi, Jiangsu, 214062, China.

Cell Biochemistry and Biophysics
|March 9, 2013
PubMed

Insights

Sunitinib reverses multidrug resistance in gastric cancer cells by inhibiting P-glycoprotein transporter function and modulating Stat3 and Bcl-2 pathways. This finding offers potential for new combination therapies against advanced gastric cancer.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Advanced gastric cancer often develops multidrug resistance (MDR).
  • Sunitinib is a multi-targeted tyrosine kinase inhibitor investigated for cancer treatment.

Purpose of the Study:

  • To investigate Sunitinib's effect on vincristine-selected multidrug-resistant gastric cancer cells (SGC7901/VCR).
  • To determine Sunitinib's potential in overcoming MDR in gastric cancer.

Main Methods:

  • Treatment of SGC7901/VCR cells with Sunitinib.
  • Assessed cytotoxicity of various chemotherapeutic agents.
  • Measured intracellular accumulation of rhodamine 123.
  • Analyzed P-glycoprotein (P-gp) expression.
  • Investigated Stat3 and Bcl-2 expression levels.

Main Results:

  • Sunitinib enhanced the cytotoxicity of adriamycin, vincristine, etoposide, 5-Fluorouracil, and cisplatin.
  • Sunitinib increased intracellular accumulation and retention of rhodamine 123 in resistant cells.
  • Sunitinib inhibited Stat3 and down-regulated Bcl-2, without affecting P-gp expression.
  • Sunitinib reversed MDR in gastric cancer cells.

Conclusions:

  • Sunitinib effectively reverses multidrug resistance in gastric cancer cells.
  • Mechanisms include inhibition of P-gp transporter function and modulation of Stat3 and Bcl-2.
  • Sunitinib holds promise for combination therapeutic strategies against gastric cancer MDR.

More Related Videos

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform06:21

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform

Published on: May 10, 2024

Related Concept Videos

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...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
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...
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...
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates these...