The oncolytic peptide LTX-315 induces cell death and DAMP release by mitochondria distortion in human melanoma cells.

Eike LM, Yang N, Rekdal Ø, Sveinbjørnsson B

Oncotarget1 Oct 2015Cited by 59 (Europe PMC)

PMID26472184PMCIDPMC4741498DOI10.18632/oncotarget.5308PepBankPUB-26472184

Summary

Host defense peptides (HDPs) are naturally occurring molecules found in most species, in which they play a significant role in the first line defense against intruding pathogens, and several HDPs have been shown to possess anticancer activity. Structure-activity relationship studies on the HDP bovine lactoferricin revealed a de novo design of a nonamer peptide LTX-315, with oncolytic properties. In the present study, we investigated the oncolytic activity of LTX-315 in human melanoma cells (A375). LTX-315 induced a rapid plasma membrane disruption and cell death within 2 hours. At a low concentration, fluorescence-labeled LTX-315 was internalized and accumulated in cytoplasmic vacuoles in close proximity to the mitochondria. The mitochondrial membrane potential was shown to depolarize as a consequence of LTX-315 treatment and at ultrastructural level, the mitochondria morphology was significantly altered. Release of danger signals (DAMPs) such as ATP, Cytochrome C and HMGB1 into the cell supernatant of cultured cells was evident minutes after peptide treatment. The oncolytic effect of LTX-315 involving perturbation of both the cell membrane and the mitochondria with subsequent release of DAMPs may highlight the ability of LTX-315 to induce complete regression and long-term protective immune responses as previously reported in experimental animal models.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study5

5 results from studies that gave the peptide. No result from this study comes from people.

01LabIn vitro (cells)Mechanism
In human melanoma cells, LTX‑315 rapidly disrupted the plasma membrane within 2 hours.
In plain wordsIn cells, LTX‑315 rapidly disrupted human melanoma cell membranes within 2 hours.
Peptide
LTX-315
Outcome
Not applicablePlasma membrane disruption
Study
humann: not reported in source
A375 melanoma cells
Outcome group
Receptor activity and mechanism · Cancer
Studied dose
Dose not stated
Source sentences
Summary
LTX-315 induced a rapid plasma membrane disruption and cell death within 2 hours.
1 context sentence(design, population, supporting numbers)
Summary · context
In the present study, we investigated the oncolytic activity of LTX-315 in human melanoma cells (A375).
Show in the study text Report a problemFND-2647218401
02LabIn vitro (cells)Activity measurement
In human melanoma cells, LTX‑315 induced cell death within 2 hours.
In plain wordsIn cells, LTX‑315 caused human melanoma cell death within 2 hours.
Peptide
LTX-315
Outcome
IncreaseCell death
Study
humann: not reported in source
A375 melanoma cells
Outcome group
Tumor growth · Cancer
Studied dose
Dose not stated
Source sentences
Summary
LTX-315 induced a rapid plasma membrane disruption and cell death within 2 hours.
1 context sentence(design, population, supporting numbers)
Summary · context
In the present study, we investigated the oncolytic activity of LTX-315 in human melanoma cells (A375).
Show in the study text Report a problemFND-2647218402
03LabIn vitro (cells)Mechanism
In human melanoma cells, LTX‑315 depolarized the mitochondrial membrane potential.
In plain wordsIn cells, LTX‑315 reduced the electrical potential across human melanoma cell mitochondrial membranes.
Peptide
LTX-315
Outcome
DecreaseMitochondrial membrane depolarization
Study
humann: not reported in source
A375 melanoma cells
Outcome group
Mitochondrial function · Cancer
Studied dose
Dose not stated
Source sentences
Summary
The mitochondrial membrane potential was shown to depolarize as a consequence of LTX-315 treatment and at ultrastructural level, the mitochondria morphology was significantly altered.
1 context sentence(design, population, supporting numbers)
Summary · context
In the present study, we investigated the oncolytic activity of LTX-315 in human melanoma cells (A375).
Show in the study text Report a problemFND-2647218403
04LabIn vitro (cells)Mechanism
In human melanoma cells, LTX‑315 significantly altered mitochondrial morphology at the ultrastructural level.
In plain wordsIn cells, LTX‑315 significantly altered the detailed structure of human melanoma cell mitochondria.
Peptide
LTX-315
Outcome
Not applicableMitochondrial morphology
Study
humann: not reported in source
A375 melanoma cells
Outcome group
Mitochondrial function · Cancer
Studied dose
Dose not stated
Source sentences
Summary
The mitochondrial membrane potential was shown to depolarize as a consequence of LTX-315 treatment and at ultrastructural level, the mitochondria morphology was significantly altered.
1 context sentence(design, population, supporting numbers)
Summary · context
In the present study, we investigated the oncolytic activity of LTX-315 in human melanoma cells (A375).
Show in the study text Report a problemFND-2647218404
05LabIn vitro (cells)Mechanism
In human melanoma cells, LTX‑315 caused release of DAMPs including ATP, Cytochrome C and HMGB1 within minutes.
In plain wordsIn cells, LTX‑315 caused human melanoma cells to release danger signals including ATP, Cytochrome C and HMGB1 within minutes.
Peptide
LTX-315
Outcome
IncreaseDAMP release
Study
humann: not reported in source
A375 melanoma cells
Outcome group
Immune response · Cancer
Studied dose
Dose not stated
Source sentences
Summary
Release of danger signals (DAMPs) such as ATP, Cytochrome C and HMGB1 into the cell supernatant of cultured cells was evident minutes after peptide treatment.
1 context sentence(design, population, supporting numbers)
Summary · context
In the present study, we investigated the oncolytic activity of LTX-315 in human melanoma cells (A375).
Show in the study text Report a problemFND-2647218405

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
27 Oct 2026, 18:20 UTC
Study results updated
Version 1
27 Oct 2026, 16:32 UTC
First added · source update from Europe PMC

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