NAD⁺ supplementation limits triple-negative breast cancer metastasis via SIRT1-P66Shc signaling.

Jiang Y, Luo Z, Gong Y, Fu Y, Luo Y

Oncogene23 Jan 2023Cited by 28 (Europe PMC)

PMID36690678DOI10.1038/s41388-023-02592-yPepBankPUB-36690678

Publisher page PubMedAsk about this study

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study6

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

01AnimalAnimal study (in vivo)Efficacy outcome
In a TNBC orthotopic patient-derived xenograft model, NAD supplementation suppressed tumor metastasis.
In plain wordsIn an animal model of triple-negative breast cancer, NAD supplementation reduced tumor metastasis.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseTumor metastasis
Study
n: not reported in source
TNBC orthotopic patient-derived xenograft model
Outcome group
Tumor growth · Cancer
Studied dose
Dose not stated
Source sentences
Summary
Here, we show that NAD⁺ supplement suppresses tumor metastasis in a TNBC orthotopic patient-derived xenograft (PDX) model.
Report a problemFND-3669067801

Studies that did not test the peptide alone5

In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking NAD+ (nicotinamide adenine dinucleotide).

02AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designMechanism
In the TNBC model, SIRT1 knockdown blocked NAD-mediated suppression of tumor metastasis.
In plain wordsIn preclinical TNBC experiments, SIRT1 gene knockdown blocked NAD-mediated reduction of tumor metastasis.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
Not applicableSIRT1 requirement for metastasis suppression
Study
n: not reported in source
TNBC model
Outcome group
Receptor activity and mechanism · Cancer
Source sentences
Summary
Sirtuin1 lysine deacetylase (SIRT1) is required for the effects since SIRT1 knockdown blocks NAD⁺-suppressed tumor metastasis.
In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).
Report a problemFND-3669067802
03AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designMechanism
In TNBC experiments, overexpression of SIRT1, implicated in NAD-mediated effects, impaired metastatic potential.
In plain wordsIn preclinical triple-negative breast cancer experiments, SIRT1 overexpression reduced metastatic potential in the NAD-related mechanism study.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseMetastatic potential with SIRT1 overexpression
Study
n: not reported in source
TNBC metastatic potential assay
Outcome group
Tumor growth · Cancer
Source sentences
Summary
Overexpression of SIRT1 effectively impairs the metastatic potential of TNBC.
1 context sentence(design, population, supporting numbers)
Summary · context
Sirtuin1 lysine deacetylase (SIRT1) is required for the effects since SIRT1 knockdown blocks NAD⁺-suppressed tumor metastasis.
In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).
Report a problemFND-3669067803
04AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designMechanism
In TNBC mechanism experiments, SIRT1 interaction with p66Shc caused p66Shc deacetylation in the NAD-associated signaling axis.
In plain wordsIn preclinical experiments, SIRT1 interaction with p66Shc caused p66Shc deacetylation in the NAD-related signaling pathway.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
Increasep66Shc deacetylation
Study
n: not reported in source
SIRT1-p66Shc interaction experiments
Outcome group
Receptor activity and mechanism · Cancer
Source sentences
Summary
Importantly, the interaction between SIRT1 and p66Shc causes the deacetylation and functional inactivation of p66Shc, which inhibits epithelial-mesenchymal transition (EMT).
1 context sentence(design, population, supporting numbers)
Summary · context
Overall, we demonstrate that NAD⁺ supplementation executes its anti-tumor function via activating the SIRT1-p66Shc axis, which highlights the preventive and therapeutic potential of SIRT1 activators as effective interventions for TNBC.
In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).
Report a problemFND-3669067804
05AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designMechanism
In TNBC mechanism experiments, SIRT1 interaction with p66Shc caused its functional inactivation in the NAD-associated signaling axis.
In plain wordsIn preclinical experiments, SIRT1 interaction with p66Shc inactivated p66Shc in the NAD-related signaling pathway.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
Decreasep66Shc functional activity
Study
n: not reported in source
SIRT1-p66Shc interaction experiments
Outcome group
Receptor activity and mechanism · Cancer
Source sentences
Summary
Importantly, the interaction between SIRT1 and p66Shc causes the deacetylation and functional inactivation of p66Shc, which inhibits epithelial-mesenchymal transition (EMT).
1 context sentence(design, population, supporting numbers)
Summary · context
Overall, we demonstrate that NAD⁺ supplementation executes its anti-tumor function via activating the SIRT1-p66Shc axis, which highlights the preventive and therapeutic potential of SIRT1 activators as effective interventions for TNBC.
In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).
Report a problemFND-3669067805
06AnimalNot a test of NAD+ (nicotinamide adenine dinucleotide) aloneOther designMechanism
In TNBC mechanism experiments, SIRT1-mediated p66Shc inactivation inhibited epithelial-mesenchymal transition in the NAD-associated signaling axis.
In plain wordsIn preclinical experiments, p66Shc inactivation inhibited epithelial-mesenchymal transition in the NAD-related signaling pathway.
Peptide
NAD+ (nicotinamide adenine dinucleotide)
Outcome
DecreaseEpithelial-mesenchymal transition
Study
n: not reported in source
SIRT1-p66Shc interaction experiments
Outcome group
Tumor growth · Cancer
Source sentences
Summary
Importantly, the interaction between SIRT1 and p66Shc causes the deacetylation and functional inactivation of p66Shc, which inhibits epithelial-mesenchymal transition (EMT).
1 context sentence(design, population, supporting numbers)
Summary · context
Overall, we demonstrate that NAD⁺ supplementation executes its anti-tumor function via activating the SIRT1-p66Shc axis, which highlights the preventive and therapeutic potential of SIRT1 activators as effective interventions for TNBC.
In this study, NAD+ (nicotinamide adenine dinucleotide) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking NAD+ (nicotinamide adenine dinucleotide).
Report a problemFND-3669067806

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
14 Oct 2026, 05:02 UTC
Study results updated
Version 1
14 Oct 2026, 01:46 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

Publication types

MeSH terms

PepBank is a research reference. Talk to a doctor before you use any peptide.