Lantana camara Induces Apoptosis by Bcl-2 Family and Caspases Activation

Eun Byeol Han1, Bo Yoon Chang, Young Suk Jung

  • 1Institute of Pharmaceutical Research and Development, College of Pharmacy, Wonkwang University, 460 Ikandae-ro, Iksan, Jeonbuk, 570-749, Republic of Korea.

Insights

A natural extract from Lantana camara shows promise as a novel breast cancer therapy. This plant extract induced cell death in human breast cancer cells by regulating apoptosis pathways.

Area of Science:

  • Phytochemistry
  • Oncology
  • Molecular Biology

Background:

  • Breast cancer remains a leading cause of cancer-related deaths globally, necessitating the development of new therapeutic strategies.
  • Drug resistance in existing cancer treatments highlights the critical need for novel anticancer agents.
  • Natural products offer a promising source for identifying new therapeutic compounds.

Purpose of the Study:

  • To investigate the anticancer potential of an extract from Lantana camara against human breast cancer cells.
  • To elucidate the molecular mechanisms underlying the cytotoxic effects of the Lantana camara extract.

Main Methods:

  • Extraction of compounds from Lantana camara.
  • Treatment of human breast cancer cell line (MCF-7) with the extract.
  • Analysis of apoptosis-related proteins including the Bcl-2 family (Bid, Bax, Bcl-2).
  • Assessment of caspase activation (caspase-8, caspase-9) and poly (ADP-ribose) polymerase (PARP) cleavage.

Main Results:

  • The Lantana camara extract demonstrated significant cell death properties in MCF-7 cells.
  • Apoptosis induction was mediated by the modulation of the Bcl-2 family proteins, with increased Bid and Bax, and decreased Bcl-2.
  • The extract influenced the cleavage of key apoptotic executioners: caspase-8, caspase-9, and PARP.

Conclusions:

  • Lantana camara extract exhibits potent anti-breast cancer activity.
  • The extract functions by initiating apoptosis through the Bcl-2 family and caspase-dependent pathways.
  • Lantana camara represents a potential source for developing novel anti-breast cancer therapeutics.

Related Concept Videos

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...
6.2K
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
8.6K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
6.1K
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
71
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
11.9K
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
3.3K