Trehalose liposomes induce apoptosis of breast tumor cells in vitro and in vivo

Ichihara, Hideaki; Kuwabara, Keiji; Matsumoto, Yōko

doi:10.1016/j.bbrc.2020.08.037

Cited by 4 publications

(5 citation statements)

References 14 publications

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“…Vertebrates do not have enzymes for the biosynthesis of trehalose but can degrade it to glucose in the small Sažetak Ključne reči: trehaloza, oksidativni stres, autofagija, terapija intestine by the enzyme trehalase found in the intestinal villi (18). Numerous studies indicate the protective effects of trehalose in neurodegenerative diseases, tumors, dry eye syndrome, infections, and cardiovascular and renal diseases (6)(7)(8)(9)(10)(11)(12)(13)(14)(20)(21)(22). The beneficial effects of trehalose result from its ability to reduce hyperinflammation, prevent aggregates and misfolded proteins accumulation, and eliminate reactive oxygen species directly, or by stabilizing antioxidant enzymes (6-9, 16, 17).…”

Section: Biochemical Properties and Biological Function Of Trehalosementioning

confidence: 99%

“…In a xenograft lung cancer model induced by the transplantation of A549 malignant cells (isolated from the lung tissue of a male with lung cancer) into mice, liposomes with trehalose reduced tumor growth and increased the level of apoptotic cells in tumor tissue (12). Recent data indicate that liposomes with trehalose also stimulate apoptosis by increasing membrane fluidity leading to the activation of caspase 3, 6 and JNK (Jun-c-Jun N-terminal kinase) signaling pathway, and inactivation of transcription factor NF-κB (nuclear factor-κB) (13). In two different melanoma cell lines (female A375, and male human melanoma cell line SK-Mel-28) trehalose significantly reduced tumor growth through autophagy -or senescence-inducing mechanisms that potentiate temozolomide and radiotherapy cytotoxicity (14).…”

Section: Trehalose As An Anticancer Agentmentioning

confidence: 99%

“…The advantageous physicochemical properties of trehalose are used in numerous fields, such as agriculture, the cosmetic industry, the food industry, and the pharmaceutical industry (1). Although vertebrates are unable to synthesize trehalose, the use of trehalose is beneficial in many diseases such as neurodegenerative diseases, tumors, dry eye syndrome, infections, and cardiovascular and renal diseases (6)(7)(8)(9)(10)(11)(12)(13)(14). Since the exact underlying mechanisms of its protective function are not well understood, certain studies have confirmed that trehalose can remove damaged proteins and aggregates and eliminate reactive oxygen species directly or by stabilizing antioxidant enzymes (6-8, 15, 16).…”

Section: Introductionmentioning

confidence: 99%

“…Since the exact underlying mechanisms of its protective function are not well understood, certain studies have confirmed that trehalose can remove damaged proteins and aggregates and eliminate reactive oxygen species directly or by stabilizing antioxidant enzymes (6-8, 15, 16). In addition, trehalose induces autophagy and reduces the inflammatory response (9), removes protein aggregates, protects neurons both in vitro and in vivo (6)(7)(8)17), and inhibits tumor cell growth and proliferation (10)(11)(12)(13)(14). In this review, the current knowledge on the potential use of trehalose as a therapeutic agent in different diseases was summarized, highlighting its beneficial effects and underlying molecular mechanisms.…”

Section: Introductionmentioning

confidence: 99%

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Trehalose as a potential therapeutic agent in different diseases

Stevanović,

Trajković,

Vučićević

2023

Medicinski podmladak

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Trehalose is a natural, non-reducing disaccharide synthesized in some bacteria, fungi, plants, and insects. Due to its advantageous physical and chemical properties, trehalose can stabilize proteins and membranes, and protect cells from desiccation, heating, and freezing. Vertebrates do not synthesize trehalose, but the beneficial effects of trehalose have been demonstrated in numerous diseases as it eliminates aggregates, misfolded proteins, and damaged organelles, and reduces hyperinflammation and oxidative stress. Trehalose induces autophagy through nuclear translocation and activation of transcription factor EB (TFEB) in an mTOR-independent manner, but increases the expression of SQSTM1/p62 and has antioxidant properties in an autophagy-independent manner. Furthermore, trehalose induces apoptosis in tumor cells by increasing membrane fluidity through the activation of caspase 3, 6 and the JNK (c-Jun N-terminal kinase) pathway. Overall, in this review, previous knowledge on the therapeutic potential of trehalose in various diseases such as dry eye syndrome, neurodegenerative diseases, and tumors, was summarized, focusing on the underlying molecular mechanisms.

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Section: Biochemical Properties and Biological Function Of Trehalosementioning

confidence: 99%

Section: Trehalose As An Anticancer Agentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Trehalose as a potential therapeutic agent in different diseases

Stevanović,

Trajković,

Vučićević

2023

Medicinski podmladak

View full text Add to dashboard Cite

show abstract

“…An example is the disaccharide trehalose that activates autophagy via the lysosomalmediated TFEB pathway [131,132]. By activating autophagy, trehalose assists the removal of several toxic misfolded proteins [131,[133][134][135], and, not surprisingly, trehalose has been proven as a therapeutic approach in in vitro and in vivo cancer models [136][137][138]. Of note, still related to PQC modulation, HSPB8 and BAG3 expression has been found to respond to some proteotoxic stress via the activation of the NF-κB transcription factor [22,73].…”

Section: Modulation Of Hspb8 Expressionmentioning

confidence: 99%

The Role of HSPB8, a Component of the Chaperone-Assisted Selective Autophagy Machinery, in Cancer

Cristofani¹,

Piccolella²,

Crippa³

et al. 2021

Cells

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The cellular response to cancer-induced stress is one of the major aspects regulating cancer development and progression. The Heat Shock Protein B8 (HSPB8) is a small chaperone involved in chaperone-assisted selective autophagy (CASA). CASA promotes the selective degradation of proteins to counteract cell stress such as tumor-induced stress. HSPB8 is also involved in (i) the cell division machinery regulating chromosome segregation and cell cycle arrest in the G0/G1 phase and (ii) inflammation regulating dendritic cell maturation and cytokine production. HSPB8 expression and role are tumor-specific, showing a dual and opposite role. Interestingly, HSPB8 may be involved in the acquisition of chemoresistance to drugs. Despite the fact the mechanisms of HSPB8-mediated CASA activation in tumors need further studies, HSPB8 could represent an important factor in cancer induction and progression and it may be a potential target for anticancer treatment in specific types of cancer. In this review, we will discuss the molecular mechanism underlying HSPB8 roles in normal and cancer conditions. The basic mechanisms involved in anti- and pro-tumoral activities of HSPB8 are deeply discussed together with the pathways that modulate HSPB8 expression, in order to outline molecules with a beneficial effect for cancer cell growth, migration, and death.

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Regulatory Mechanism of Neurotrophin Receptor-Interacting Melanoma Antigen Coding Gene Homolog (NRAGE) Gene Methylation on Apoptosis of Breast Cancer Cell Under Tyrosine Kinases/Methyl Ethyl Ketone/Extracellular Regulated Protein Kinases Signaling Pathway

Wen

2022

j biomater tissue eng

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The aim of this study was to discover the influence of Neurotrophin receptor-interacting MAGE homolog (NRAGE) gene methylation on proliferation (Pro) and apoptosis (Apo) of breast cancer cell (BCC), and its influence on TrkA/MEK/ERK signaling. BCC lines MCF-7, MDA-MB-231, and normal mammary gland cell (MGC) MCF-10 were selected. Expression of NRAGE mRNA and methylation level in cells was analyzed via reverse transcription-polymerase chain reaction (RT-PCR) and methylation-specific PCR. Different concentrations (0, 5, 10 mol/L) of DNA methylase inhibitor 5-aza-2′-deoxycytidine (5-Aza-CdR) were adopted to treat the BCC cell line. With dimethyl sulfoxide (DMSO) treatment as control, cell count, 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry, and Western blot were adopted to detect the Pro, Apo, relative expression (REP) of Apo-related proteins Bcl-2, Bax, and target proteins TrkA, MEK, and ERK1/2 after different treatments. The results showed that NRAGE mRNA level in MDA-MB-231 and MCF-7 was notably reduced versus MCF-10 (P < 0.05), and they could express methylated NRAGE specifically. 5-Aza-CdR can increase unmethylated NRAGE’s expression in BCC. Cell Pro level of the 5 and 10 mol/L treatments was greatly inhibited than DMSO and 0 mol/L treatments (P < 0.05). Apo rate and Apo-related proteins Bcl-2 and Bax increased obviously (P < 0.05). In addition, the phosphorylation levels of TrkA in the 5 and 10 mol/L treatments were considerably reduced (P < 0.05), while that in MEK and ERK1/2 was remarkably increased (P < 0.05). In short, NRAGE methylation can inhibit BCC’s Pro and regulate BCC’s Pro and Apo through TrkA/MEK/ERK signaling.

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Trehalose liposomes induce apoptosis of breast tumor cells in vitro and in vivo

Cited by 4 publications

References 14 publications

Trehalose as a potential therapeutic agent in different diseases

Trehalose as a potential therapeutic agent in different diseases

The Role of HSPB8, a Component of the Chaperone-Assisted Selective Autophagy Machinery, in Cancer

Regulatory Mechanism of Neurotrophin Receptor-Interacting Melanoma Antigen Coding Gene Homolog (NRAGE) Gene Methylation on Apoptosis of Breast Cancer Cell Under Tyrosine Kinases/Methyl Ethyl Ketone/Extracellular Regulated Protein Kinases Signaling Pathway

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