Related Experiment Video

Updated: Dec 25, 2025

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

19.1K

Piscidin-1 Induces Apoptosis via Mitochondrial Reactive Oxygen Species-Regulated Mitochondrial Dysfunction in Human

Meng-Hsuan Cheng1,2,3, Chieh-Yu Pan4, Nan-Fu Chen5,6

  • 1Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, 80756, Taiwan.

Scientific Reports
|March 21, 2020
PubMed

Insights

Piscidin-1, a marine antimicrobial peptide, effectively targets osteosarcoma cells by inducing apoptosis and mitochondrial dysfunction. This peptide shows promise as a novel therapeutic agent for bone cancer treatment.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Osteosarcoma (OSA) is a primary bone cancer predominantly affecting children, with current treatments yielding suboptimal outcomes.
  • Marine antimicrobial peptides (AMPs) are explored for their therapeutic potential, including anti-cancer properties.
  • The specific effects of Piscidin-1 on mitochondrial function in OSA remain largely uncharacterized.

Purpose of the Study:

  • To investigate the impact of Piscidin-1 on mitochondrial reactive oxygen species (mtROS) and apoptosis in osteosarcoma cells.
  • To determine the selectivity of Piscidin-1 against OSA cells compared to other cancer types and non-cancerous cells.

Main Methods:

  • In vitro assessment of Piscidin-1's cytotoxic effects on various cancer and non-cancer cell lines.
  • Analysis of mtROS levels, apoptosis markers, mitochondrial transmembrane potential, and adenosine 5'-triphosphate (ATP) production in OSA cells treated with Piscidin-1.
  • Evaluation of the protective effect of the antioxidant mitoTempo against Piscidin-1-induced apoptosis.

Main Results:

  • Piscidin-1 demonstrated significant cytotoxicity towards OSA cells, with minimal impact on lung, ovarian, and non-cancer cells.
  • Piscidin-1 treatment led to increased apoptosis in OSA cells, accompanied by regulation of mtROS.
  • Piscidin-1 reduced manganese superoxide dismutase, mitochondrial transmembrane potential, and ATP production, indicating induced mitochondrial dysfunction.

Conclusions:

  • Piscidin-1 effectively induces apoptosis and mitochondrial dysfunction in osteosarcoma cells.
  • The observed effects suggest Piscidin-1's potential as a targeted therapeutic agent for osteosarcoma.
  • MitoTempo mitigated Piscidin-1-induced apoptosis, further supporting the role of mitochondrial pathways in its mechanism of action.

More Related Videos

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer04:20

Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer

Published on: February 9, 2024

1.3K
Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

781

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...
8.0K
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...
7.8K
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...
13.5K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.1K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.0K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
11.6K