Preparation of a PEGylated liposome that co-encapsulates l-arginine and doxorubicin to achieve a synergistic anticancer effect

Haitao Feng; Jeong-Hun Kang; Song Qi; Akihiro Kishimura; Takeshi Mori; Yoshiki Katayama

doi:10.1039/d1ra06514a

ANTICANCER EFFECT OF UVARIA GENUS

Journal of Medicine and Pharmacy ◽

10.34071/jmp.2013.6.16 ◽

2014 ◽

pp. 98-101

Author(s):

Thi Bich Hien Le ◽

Viet Duc Ho ◽

Thi Hoai Nguyen

Keyword(s):

Biological Activities ◽

Current Trend ◽

Healthcare Systems ◽

Chemical Compositions ◽

Cancer Therapies ◽

Pharmacological Effects ◽

Anticancer Effect ◽

Anti Cancer ◽

Tropical Areas ◽

Cancer Activity

Nowadays, cancer treatment has been a big challenge to healthcare systems. Most of clinical anti-cancer therapies are toxic and cause adverse effects to human body. Therefore, current trend in science is seeking and screening of natural compounds which possess antineoplastic activities to utilize in treatment. Uvaria L. - Annonaceae includes approximately 175 species spreading over tropical areas of Asia, Australia, Africa and America. Studies on chemical compositions and pharmacological effects of Uvaria showed that several compound classes in this genus such as alkaloid, flavonoid, cyclohexen derivaties, acetogenin, steroid, terpenoid, etc. indicate considerable biological activities, for example anti-tumor, anti-cancer, antibacterial, antifungal, antioxidant, etc. Specifically, anti-cancer activity of fractions of extract and pure isolated compounds stands out for cytotoxicity against many cancer cell lines. This study provides an overview of anti-cancer activity of Uvaria and suggests a potential for further studies on seeking and developing novel anti-cancer compounds. Key words: Anti-cancer, Uvaria.

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Anticancer and Differentiation Properties of the Nitric Oxide Derivative of Lopinavir in Human Glioblastoma Cells

Molecules ◽

10.3390/molecules23102463 ◽

2018 ◽

Vol 23 (10) ◽

pp. 2463 ◽

Cited By ~ 26

Author(s):

Maria Basile ◽

Emanuela Mazzon ◽

Tamara Krajnovic ◽

Dijana Draca ◽

Eugenio Cavalli ◽

...

Keyword(s):

Nitric Oxide ◽

Cell Types ◽

Hiv Protease ◽

Hiv Protease Inhibitors ◽

In Vitro Growth ◽

Anticancer Effect ◽

Human Gbm ◽

Oxide Derivative ◽

Primary Malignant Brain Tumor

Glioblastoma (GBM) is the most frequent and deadly form of primary malignant brain tumor among adults. A promising emerging approach for GBM treatment may be offered from HIV protease inhibitors (HIV-PIs). In fact, in addition to their primary pharmacological activity in the treatment of HIV infection, they possess important anti-neoplastic effects. According to previous studies, the addition of a nitric oxide (NO) donating group to parental compounds can reduce their toxicity and enhance the anticancer action of various compounds, including HIV-PIs. In this study we compared the effects of the HIV-PI Lopinavir (Lopi) and of its NO-derivative Lopinavir-NO (Lopi-NO) on the in vitro growth of LN-229 and U-251 human GBM cell lines. Lopi-NO reduced the viability of LN-229 and U-251 cells at significantly lower concentrations than the parental drug. In particular, Lopi-NO inhibited tumor cell proliferation and induced the differentiation of U-251 cells toward an astrocyte-like phenotype without triggering significant cell death in both cell types. The anticancer effect of Lopi-NO was persistent even upon drug removal. Furthermore, Lopi-NO induced strong autophagy that did not appear to be related to its chemotherapeutic action. Overall, our results suggest that Lopi-NO could be a potential effective anticancer drug for GBM treatment.

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Protein kinase inhibitor-based cancer therapies: Considering the potential of nitric oxide (NO) to improve cancer treatment

Biochemical Pharmacology ◽

10.1016/j.bcp.2020.113855 ◽

2020 ◽

Vol 176 ◽

pp. 113855 ◽

Cited By ~ 2

Author(s):

Silvia Ghione ◽

Nesrine Mabrouk ◽

Catherine Paul ◽

Ali Bettaieb ◽

Stéphanie Plenchette

Keyword(s):

Nitric Oxide ◽

Protein Kinase ◽

Cancer Treatment ◽

Kinase Inhibitor ◽

Protein Kinase Inhibitor ◽

Cancer Therapies

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Synergistic Anticancer Effect of Gemcitabine Combined With Impressic Acid or Acankoreanogein in Panc-1 Cells by Inhibiting NF-κB and Stat 3 Activation

Natural Product Communications ◽

10.1177/1934578x20974239 ◽

2020 ◽

Vol 15 (12) ◽

pp. 1934578X2097423

Author(s):

Sen Jiang ◽

Dong-Li Li ◽

Jie Chen ◽

Xi Zheng ◽

Pan-Pan Wu ◽

...

Keyword(s):

Biological Activities ◽

Cancer Therapies ◽

Nuclear Factor ◽

Anticancer Effect ◽

Acanthopanax Trifoliatus ◽

Mechanistic Investigation ◽

Improvement Effect ◽

Induction Of Apoptosis ◽

Light Chain Enhancer ◽

Important Activity

Natural products have presented potentiality to improve the outcomes of cancer therapies. Impressic acid (E12-1) and acankoreanogein (E13-1), important activity compounds in Acanthopanax trifoliatus (L.) Merr., show widely biological activities. In this study, we isolated E12-1 and E13-1 from Acanthopanax trifoliatus (L.) Merr., and investigated their improvement effect in gemcitabine (GEM) treatment in Panc-1 cells. The results showed that GEM in combination with E12-1 or E13-1 showed stronger inhibition on the growth and induction of apoptosis in Panc-1 cells compared to GEM, E12-1, or E13-1 alone. GEM in combination with E12-1or E13-1 also strongly inhibited cell migration. Mechanistic investigation showed that GEM in combination with E12-1or E13-1 effectively inhibited the activition of nuclear factor kappa-light-chain-enhancer of activated B cells and Stat 3. Overall, GEM in combination with E12-1 or E13-1 might be an effective strategy for the prevention of prostate cancer.

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Enhancing doxorubicin anticancer activity with a novel polymeric platform photoreleasing nitric oxide

Biomaterials Science ◽

10.1039/c9bm01644a ◽

2020 ◽

Vol 8 (5) ◽

pp. 1329-1344 ◽

Cited By ~ 8

Author(s):

Federica Sodano ◽

Robert J. Cavanagh ◽

Amanda K. Pearce ◽

Loretta Lazzarato ◽

Barbara Rolando ◽

...

Keyword(s):

Nitric Oxide ◽

Anticancer Activity ◽

Treatment Modalities ◽

Cancer Therapies ◽

No Release ◽

New Treatment ◽

Polymeric Conjugate

Combination of Doxorubicin with light-regulated NO release achieved through formulation strategy of tailored polymeric conjugate nanoparticles may open new treatment modalities to improve cancer therapies.

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A Hepatitis B Virus-Derived Peptide Exerts an Anticancer Effect via TNF/iNOS-producing Dendritic Cells in Tumor-Bearing Mouse Model

Cancers ◽

10.3390/cancers13030407 ◽

2021 ◽

Vol 13 (3) ◽

pp. 407

Author(s):

Soo-Bin Yang ◽

Mi-Hyun Lee ◽

Bo-Ram Kim ◽

Yu-Min Choi ◽

Bum-Joon Kim

Keyword(s):

Nitric Oxide ◽

Dendritic Cells ◽

Hepatitis B Virus ◽

Hepatitis B ◽

Mouse Model ◽

Checkpoint Inhibitors ◽

Dependent Manner ◽

Anticancer Effect ◽

B Virus

Recently, we reported a 6-mer hepatitis B virus (HBV)-derived peptide, Poly6, that exerts antiviral effects against human immunodeficiency virus type 1 (HIV-1). Here, we explored the immunotherapeutic potential of Poly6 via its administration into dendritic cells (DCs) in a mouse model. Our data revealed that Poly6 treatment led to enhanced production of tumor necrosis factor alpha (TNF-α) and inducible nitric oxide synthase (iNOS)-producing DCs (Tip-DCs) in a type 1 interferon (IFN-I)-dependent manner via the induction of mitochondrial stress. Poly6 treatment in mice implanted with MC38 cells, a murine colon adenocarcinoma line, led to attenuated tumor formation, primarily due to direct cell death induced by Tip-DC mediated nitric oxide (NO) production and indirect killing by Tip-DC mediated cluster of differentiation 8 (CD8) cytotoxic T lymphocyte (CTL) activation via CD40 activation. Moreover, Poly6 treatment demonstrated an enhanced anticancer effect with one of the checkpoint inhibitors, the anti PD-L1 antibody. In conclusion, our data reveal that Poly6 treatment elicits an antitumor immune response in mice, possibly through NO-mediated oncolytic activity via Tip-DC activation and Tip-DC mediated CTL activation. This suggests that Poly6 represents a potential adjuvant for cancer immunotherapy by enhancing the anticancer effects of immune checkpoint inhibitors.

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NMR-Based metabolomic analysis of the anticancer effect of metformin on cholangiocarcinoma cells

10.21203/rs.2.22216/v1 ◽

2020 ◽

Author(s):

Jin Zhang ◽

Caihua Hang ◽

Wei Shao ◽

Wengang Li ◽

Donghai Lin

Keyword(s):

Amino Acids ◽

Tca Cycle ◽

Essential Amino Acids ◽

Cancer Therapies ◽

Dependent Manner ◽

Metformin Treatment ◽

Anticancer Effect ◽

Multivariate Statistical ◽

Cell Viability Assay ◽

Viability Assay

Abstract Background Metformin is a widely prescribed anti-diabetes drug with potential utilities for cancer therapies. Several previous studies have related metformin to the reduced risk of cholangiocarcinoma (CCA), highlighting its potentialities for the treatments of CCA. Methods In this study, cell viability assay and colony formation assay were used to test the inhibition effect of metformin on Mz-ChA-1 cells. The NMR-based metabonomic analysis was conduct to compare the differences between the metformin-treated (Met) and control (Ctrl) groups of the Mz-ChA-1 cells. Significant metabolites were identified from multivariate statistical analysis of 1D 1 H-NMR spectral data, and differential metabolites were identified from the pair-wise t-test of the metabolite levels. Significantly altered metabolic pathways were identified based on characteristic metabolites which were determined by a combination of the significant metabolites and differential metabolites. Results Here, we demonstrated that metformin treatment could inhibit the proliferation of the CCA cell line Mz-ChA-1 in a dose-dependent manner. The NMR-based metabonomic analysis showed a distinct discrimination between the Met and Ctrl groups of the Mz-ChA-1 cells. Moreover, The Met group exhibited promoted glycolysis and suppressed TCA cycle compared with the Ctrl group. While metformin treatment decreased non-essential amino acids, it also increased essential amino acids and UDP-GlcNAc, implying the occurrence of autophagy and cell cycle arrest in metformin-treated CAA cells . Conclusions This work provides a mechanistic understanding of the anticancer effect of metformin on CAA, and is beneficial to the further development of metformin as an anticancer drug

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“Good Fashion is Evolution, Not Revolution” - Methods to Enhance Existing Anticancer Medicines, Primarily with the Use of Transition Metal

Anti-Cancer Agents in Medicinal Chemistry ◽

10.2174/1871520618666171129213132 ◽

2018 ◽

Vol 18 (4) ◽

pp. 476-487

Author(s):

Magdalena Guzowska ◽

Monika Kalinowska ◽

Wlodzimierz Lewandowski

Keyword(s):

Transition Metal ◽

Anticancer Drugs ◽

Small Rnas ◽

Chemical Compounds ◽

Electronic Charge ◽

Cancer Therapies ◽

Anticancer Effect ◽

Electronic Charge Density ◽

Anticancer Properties ◽

The Relationship

The constant search for successful cancer therapies lasts for decades. Apart from the huge scientific effort and enormous sum of spent money, only a small amount of newly developed medicines move into clinical use (only 94 registered anticancer drugs in the last 12 years). Anticancer regimes are still overcome by drugs invented over 50 years ago such as cisplatin and doxorubicin. Significant progress in the development of improved anticancer drugs was made due to multiple studies on the relationship between the molecular structure of chemical compounds and their cytostatic activity. A number of ligands (mainly organic) with quite effective anticancer properties are known, but they show insufficient activity, selectivity and multidrug resistance. Formation of transition metal – ligand complexes (with proven anticancer effect) changes the properties of the latter. The factors that affect the cytotoxic properties of metal complexes are: the type of ligand and metal, the nature of the connection between metal and ligand, and the distribution of electronic charge density in the formed complexes. Here, we report the recent efforts to improve existing compounds with confirmed anticancer activity. They seem to be unappreciated as their effects appear to be less spectacular than that of targeted anticancer drugs (i.e. based on antibodies or small RNAs).

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Nuclear Magnetic Resonance-Based Metabolomic Analysis of the Anticancer Effect of Metformin Treatment on Cholangiocarcinoma Cells

Frontiers in Oncology ◽

10.3389/fonc.2020.570516 ◽

2020 ◽

Vol 10 ◽

Author(s):

Jin Zhang ◽

Caihua Hang ◽

Ting Jiang ◽

Shenghui Yi ◽

Wei Shao ◽

...

Keyword(s):

Molecular Mechanisms ◽

Umbilical Vein ◽

Cancer Therapies ◽

Metformin Treatment ◽

Anticancer Effect ◽

Multivariate Statistical ◽

Cycle Arrest ◽

Diabetes Drug ◽

Umbilical Vein Endothelial Cells ◽

And Control

Metformin is a widely prescribed anti-diabetes drug with potential utilities for cancer therapies. Several studies have related metformin to the reduced risk of cholangiocarcinoma (CCA), highlighting its potentialities for the treatments of CCA. However, the underlying molecular mechanisms remain elusive. Here, we demonstrated that metformin treatment could inhibit proliferations of the human CCA cell lines Mz-ChA-1 and QBC939 in dose-dependent manners. The NMR-based metabonomic analyses showed distinct discriminations between the metformin-treated (Met) and control (Ctrl) groups of both CCA cells. Characteristic metabolites were identified by a combination of multivariate statistical analysis of 1D 1H-NMR spectral data and the pair-wise t-test of metabolite levels. We then identified four significantly altered metabolic pathways based on the characteristic metabolites, including glucose metabolism, oxidative stress-related metabolism, energy metabolism, and amino acids metabolism. Comparing CCA cells with normal human umbilical vein endothelial cells (HUVECs), we found that metformin treatment profoundly promoted glycolysis and specifically increased the levels of BCAAs and UDP-GlcNAc, implying the occurrence of autophagy and cell cycle arrest in metformin-treated CAA cells. This work provides a mechanistic understanding of the anticancer effect of metformin treatment on CAA cells, and is beneficial to further developments of metformin as an anticancer drug.

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