Related Experiment Video

Updated: May 13, 2026

Murine Model for Non-invasive Imaging to Detect and Monitor Ovarian Cancer Recurrence
08:55

Murine Model for Non-invasive Imaging to Detect and Monitor Ovarian Cancer Recurrence

Published on: November 2, 2014

Immune escape of AKT overexpressing ovarian cancer cells

Jens C Hahne1, Susanne R Meyer, Stepan Gambaryan

  • 1Department of Gynecology, University Hospital of Würzburg, D-97080 Würzburg, Germany.

International Journal of Oncology
|March 8, 2013
PubMed

Insights

Platinum-resistant ovarian cancer cells evade natural killer (NK) cell attacks. This resistance is linked to increased anti-apoptotic genes and soluble MICA/B, hindering NK cell-mediated killing and suggesting new immunotherapy targets.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Platinum-resistance is a major challenge in ovarian cancer treatment.
  • Immunotherapy is a promising strategy due to survival's link to immunological parameters.
  • Understanding tumor-immune cell interactions is crucial for developing new treatments.

Purpose of the Study:

  • To investigate interactions between platinum-sensitive and platinum-resistant ovarian cancer cells and natural killer (NK) cells.
  • To elucidate the molecular mechanisms underlying NK cell resistance in ovarian cancer.

Main Methods:

  • Utilized a modified FATAL assay to determine NK cell-mediated killing efficiency.
  • Analyzed gene expression of pro- and anti-apoptotic factors via RT-PCR.
  • Assessed NK cell receptor recognition ligands using flow cytometry.

Main Results:

  • Platinum-resistant ovarian cancer cells (A2780cis) showed reduced susceptibility to NK cell-mediated lysis compared to platinum-sensitive cells (A2780).
  • A2780cis cells exhibited increased expression of anti-apoptotic genes, specifically CIAP-1 and -2.
  • Elevated levels of soluble MICA/B were observed in platinum-resistant cells, contributing to lower NK cell killing rates.

Conclusions:

  • Platinum resistance in ovarian cancer involves mechanisms that shield cancer cells from NK cell immunity.
  • Increased anti-apoptotic gene expression and soluble MICA/B are key factors in this resistance.
  • These findings highlight potential targets for novel immunotherapeutic strategies against platinum-resistant ovarian cancer.

More Related Videos

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts10:27

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

An Ex Vivo Model of Ovarian Cancer Peritoneal Metastasis Using Human Omentum05:42

An Ex Vivo Model of Ovarian Cancer Peritoneal Metastasis Using Human Omentum

Published on: January 26, 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...
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...
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...
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...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...