Lycopene sensitizes the cervical cancer cells to cisplatin via targeting nuclear factor- kappa B (NF-κB) pathway

Oktay Halİt Aktepe1, Taha Koray Şahin2, Gürkan Güner1

  • 1Department of Medical Oncology, Faculty of Medicine, Hacettepe University, Ankara, Turkey

Abstract

Insights

Lycopene enhances cisplatin

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Lycopene exhibits anticancer properties across various tumor types.
  • Mechanisms of lycopene in human cervical cancer require further elucidation.
  • Cervical cancer remains a significant global health concern.

Purpose of the Study:

  • To investigate the anticancer efficacy of lycopene in human cervical carcinoma (HeLa) cells.
  • To determine the synergistic effects of lycopene with cisplatin.
  • To elucidate the molecular mechanisms underlying lycopene's action.

Main Methods:

  • HeLa cells were treated with lycopene (10 μM) and cisplatin (1 μM) alone and in combination.
  • Cell viability was assessed using MTS assay.
  • Western blotting analyzed protein expression of NF-κB, Bax, Nrf2, and Bcl-2.

Main Results:

  • Lycopene synergistically enhanced cisplatin's inhibitory effect on HeLa cell viability (37.4% viability).
  • Lycopene increased Bax and Nrf2 expression while decreasing Bcl-2 expression.
  • Lycopene suppressed NF-κB signaling and modulated Nrf2 pathways.

Conclusions:

  • Lycopene sensitizes cervical cancer cells to cisplatin by inhibiting viability and altering apoptosis-related protein expression.
  • Lycopene's anticancer effects involve suppressing NF-κB-mediated inflammation and modulating Nrf2-mediated oxidative stress.
  • Lycopene combined with cisplatin may improve cervical cancer treatment outcomes.

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...
8.5K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
7.9K
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...
5.4K
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic...
5.1K
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
9.6K