Nisin ZP, an Antimicrobial Peptide, Induces Cell Death and Inhibits Non-Small Cell Lung Cancer (NSCLC) Progression in vitro in 2D and 3D Cell Culture

Patil, Suyash M.; Kunda, Nitesh K.

doi:10.1007/s11095-022-03220-2

Cited by 18 publications

(8 citation statements)

References 31 publications

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“…The cytotoxic effects of numerous AMPs on different tumor cell lines have been reported previously (Cheng et al, 2020;Lee et al, 2021;Athira et al, 2022;Jafari et al, 2022;Patil and Kunda, 2022). These AMPs contain several cationic and hydrophobic amino acids and were found to be involved in various anticancer activities.…”

Section: Structure Of Ll-37mentioning

confidence: 63%

Renovation as innovation: Repurposing human antibacterial peptide LL-37 for cancer therapy

Zhu

Zhang

et al. 2022

Front. Pharmacol.

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In many organisms, antimicrobial peptides (AMPs) display wide activities in innate host defense against microbial pathogens. Mammalian AMPs include the cathelicidin and defensin families. LL37 is the only one member of the cathelicidin family of host defense peptides expressed in humans. Since its discovery, it has become clear that they have pleiotropic effects. In addition to its antibacterial properties, many studies have shown that LL37 is also involved in a wide variety of biological activities, including tissue repair, inflammatory responses, hemotaxis, and chemokine induction. Moreover, recent studies suggest that LL37 exhibits the intricate and contradictory effects in promoting or inhibiting tumor growth. Indeed, an increasing amount of evidence suggests that human LL37 including its fragments and analogs shows anticancer effects on many kinds of cancer cell lines, although LL37 is also involved in cancer progression. Focusing on recent information, in this review, we explore and summarize how LL37 contributes to anticancer effect as well as discuss the strategies to enhance delivery of this peptide and selectivity for cancer cells.

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Section: Structure Of Ll-37mentioning

confidence: 63%

Renovation as innovation: Repurposing human antibacterial peptide LL-37 for cancer therapy

Zhu

Zhang

et al. 2022

Front. Pharmacol.

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“…The antimicrobial peptide Ranatuerin-2PLx extracted from skin secretions by Chen et al has the effect of inhibiting the proliferation of a variety of tumor cells(28). Patil et al found that the antimicrobial peptide Nisin ZP can inhibit A549 cell proliferation through non-membrane lysis pathway, mitochondrial membrane depolarization and increase reactive oxygen species (ROS) production, while signi cantly inhibiting three-dimensional spheroid growth and cell viability of A549 cells, showing potential therapeutic effects on highly metastatic non-small cell lung cancer (29). Therefore, CCK-8 cytotoxicity assay was used to detect the effect of Merecidin on the proliferation of TNBC cells.…”

Section: Discussionmentioning

confidence: 99%

The antimicrobial peptide Merecidin Inhibit the metastasis of triple-negative breast cancer by obstructing EMT via miR-30d-5p/vimentin

song,

ma,

et al. 2023

Preprint

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LL-37 is an important innate immune effector molecule with great potential in antitumor therapy. Merecidin retains the most active active fragment in LL-37 with antitumor biological activity and stability. This study mainly explores the inhibitory effect of antimicrobial peptide Merecidin on triple-negative breast cancer (TNBC) cells and the mechanism of inhibiting the epithelial-mesenchymal transition (EMT) by regulating miR-30d-5p/vimentin, thereby inhibiting breast cancer metastasis. The results showed that the Merecidin was able to inhibit the proliferation, migration and invasion capacity and EMT of TNBC cells (MDA-MB-231 and MDA-MB-468) in vitro. Laser confocal localization showed that Merecidin was mainly localized in the cytoplasm of TNBC cells, and the RT-qPCR results showed that miR-30d-5p was poorly expressed in TNBC cells, and Merecidin could significantly upregulate the expression of miR-30d-5p. In addition, the Dual-luciferase reporter and q-PCR results confirmed that miR-30d-5p binds to vimentin and negatively regulates vimentin. At the same time, pull down experiments showed that Merecidin can bind to vimentin in vitro. In addition, scratch experiments and Transwell experiments showed that miR-30d-5p inhibited the migration and invasion ability of TNBC cells, while vimentin promoted the migration and invasion ability of TNBC cells. Finally, down-regulation of miR-30d-5p or overexpression of vimentin could partially counteract the inhibitory effect of Merecidin on TNBC cell migration, invasion ability and EMT. In the nude mouse MDA-MB-231 subcutaneous tumor model, Merecidin significantly inhibited tumor growth and cell proliferation and upregulated the expression of miR-30d-5p in tumor tissues, inhibiting the expression of vimentin and EMT. In conclusion, Merecidin can effectively inhibit the proliferation, migration and invasion ability of TNBC cancer cells; localization in the cytoplasm; By regulating miR-30d-5p/vimentin, it can effectively hinder the EMT process, thereby effectively inhibiting the migration and invasion of TNBC cells. These findings provide new insights into the molecular function of Merecidin, suggesting its potential as a therapeutic agent for TNBC.

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“…The downstream ERK/P90RSK signaling pathway of TIMM50 (translocase of the inner mitochondrial membrane 50) can enhance the tumor proliferation and invasion of NSCLC via enhancing phosphorylation [ 163 ]. With the inhibition of Nrf2 expression and mitochondrial respiratory chain complex in LSCC, (+)-usnic acid can induce ROS-dependent apoptosis and thus a prospective clinical trial for this subtype of NSCLC [ 164 ]. The predicted nuclear-mitochondrial cross-talks are associated with the alteration of mitochondrial genes.…”

Section: Blocking Common Nsclc Metabolic Pathways As Anti-nsclcmentioning

confidence: 99%

Energy metabolism as the hub of advanced non-small cell lung cancer management: a comprehensive view in the framework of predictive, preventive, and personalized medicine

Bajinka,

Ouedraogo,

Golubnitschaja

et al. 2024

EPMA Journal

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Energy metabolism is a hub of governing all processes at cellular and organismal levels such as, on one hand, reparable vs. irreparable cell damage, cell fate (proliferation, survival, apoptosis, malignant transformation etc.), and, on the other hand, carcinogenesis, tumor development, progression and metastazing versus anti-cancer protection and cure. The orchestrator is the mitochondria who produce, store and invest energy, conduct intracellular and systemically relevant signals decisive for internal and environmental stress adaptation, and coordinate corresponding processes at cellular and organismal levels. Consequently, the quality of mitochondrial health and homeostasis is a reliable target for health risk assessment at the stage of reversible damage to the health followed by cost-effective personalized protection against health-to-disease transition as well as for targeted protection against the disease progression (secondary care of cancer patients against growing primary tumors and metastatic disease).The energy reprogramming of non-small cell lung cancer (NSCLC) attracts particular attention as clinically relevant and instrumental for the paradigm change from reactive medical services to predictive, preventive and personalized medicine (3PM). This article provides a detailed overview towards mechanisms and biological pathways involving metabolic reprogramming (MR) with respect to inhibiting the synthesis of biomolecules and blocking common NSCLC metabolic pathways as anti-NSCLC therapeutic strategies. For instance, mitophagy recycles macromolecules to yield mitochondrial substrates for energy homeostasis and nucleotide synthesis. Histone modification and DNA methylation can predict the onset of diseases, and plasma C7 analysis is an efficient medical service potentially resulting in an optimized healthcare economy in corresponding areas. The MEMP scoring provides the guidance for immunotherapy, prognostic assessment, and anti-cancer drug development. Metabolite sensing mechanisms of nutrients and their derivatives are potential MR-related therapy in NSCLC. Moreover, miR-495-3p reprogramming of sphingolipid rheostat by targeting Sphk1, 22/FOXM1 axis regulation, and A2 receptor antagonist are highly promising therapy strategies. TFEB as a biomarker in predicting immune checkpoint blockade and redox-related lncRNA prognostic signature (redox-LPS) are considered reliable predictive approaches.Finally, exemplified in this article metabolic phenotyping is instrumental for innovative population screening, health risk assessment, predictive multi-level diagnostics, targeted prevention, and treatment algorithms tailored to personalized patient profiles—all are essential pillars in the paradigm change from reactive medical services to 3PM approach in overall management of lung cancers. This article highlights the 3PM relevant innovation focused on energy metabolism as the hub to advance NSCLC management benefiting vulnerable subpopulations, affected patients, and healthcare at large.

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Nisin ZP, an Antimicrobial Peptide, Induces Cell Death and Inhibits Non-Small Cell Lung Cancer (NSCLC) Progression in vitro in 2D and 3D Cell Culture

Cited by 18 publications

References 31 publications

Renovation as innovation: Repurposing human antibacterial peptide LL-37 for cancer therapy

Renovation as innovation: Repurposing human antibacterial peptide LL-37 for cancer therapy

The antimicrobial peptide Merecidin Inhibit the metastasis of triple-negative breast cancer by obstructing EMT via miR-30d-5p/vimentin

Energy metabolism as the hub of advanced non-small cell lung cancer management: a comprehensive view in the framework of predictive, preventive, and personalized medicine

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