Peroxidase‐Like Nanozymes Induce a Novel Form of Cell Death and Inhibit Tumor Growth In Vivo

2020 ◽  
Vol 30 (21) ◽  
pp. 2000647 ◽  
Author(s):  
Peixia Wang ◽  
Shili Liu ◽  
Mingxiang Hu ◽  
Hongwei Zhang ◽  
Demin Duan ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Growth ◽  
Inhibit Tumor Growth

Raspberry pulp polysaccharides inhibit tumor growth via immunopotentiation and enhance docetaxel chemotherapy against malignant melanoma in vivo

2015 ◽  
Vol 6 (9) ◽  
pp. 3022-3034 ◽  
Author(s):  
Yong-Jing Yang ◽  
Han-Mei Xu ◽  
You-Rui Suo
Keyword(s):  
Malignant Melanoma ◽  
Antitumor Activity ◽  
Tumor Growth ◽  
Antitumor Effect ◽  
Inhibit Tumor Growth ◽  
Docetaxel Chemotherapy

Raspberry pulp polysaccharides exhibit antitumor activity in vivo against malignant melanoma through immunopotentiation and enhance the antitumor effect of docetaxel.

Spice-derived phenolic, malabaricone B induces mitochondrial damage in lung cancer cellsviaa p53-independent pathway

2018 ◽  
Vol 9 (11) ◽  
pp. 5715-5727 ◽  
Author(s):  
Mrityunjay Tyagi ◽  
Biswanath Maity ◽  
Bhaskar Saha ◽  
Ajay Kumar Bauri ◽  
Mahesh Subramanian ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Tumor Growth ◽  
Lung Tumor ◽  
Mitochondrial Damage

The spice-derived phenolic, malabaricone B induces mitochondrial cell death and reduces lung tumor growthin vivo.

Cyclometalated iridium(iii) complexes induce mitochondria-derived paraptotic cell death and inhibit tumor growthin vivo

2018 ◽  
Vol 47 (20) ◽  
pp. 6942-6953 ◽  
Author(s):  
Liang He ◽  
Kang-Nan Wang ◽  
Yue Zheng ◽  
Jian-Jun Cao ◽  
Ming-Fang Zhang ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Growth ◽  
Mitochondrial Dysfunction

A potent anticancer Ir(iii) complex induces paraptotic cell death by causing mitochondrial dysfunction rapidly and inhibits tumor growth significantlyin vivo.

miR-15a regulation of endothelial radiation sensitivity in colorectal cancer.

2018 ◽  
Vol 36 (4_suppl) ◽  
pp. 709-709
Author(s):  
Shushan Rajesh Rana ◽  
Cristina Espinosa ◽  
Rebecca Ruhl ◽  
Latroy Robinson ◽  
Charles R. Thomas ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Death ◽  
Tumor Growth ◽  
Tumor Cell ◽  
Background Radiation ◽  
Acid Sphingomyelinase ◽  
High Dose ◽  
Tumor Cell Death ◽  
Caspase 1

709 Background: Radiation dose escalation causes significant changes within the tumor microenvironment (TME) to enhance tumor cell death including altered microRNA (miR) levels. Among endothelial miRs, we identified miR-15a exhibits dose dependent differential regulation. miR-15a targets a key determinant of endothelial cell (EC) radiosensitivity, acid sphingomyelinase (SMPD1), an enzyme that drives rapid EC apoptosis via enhanced ceramide production. In colorectal cancer (CRC) (n = 182 patients), high miR-15a is associated with worse 5-year progression free and overall survival. miR-15a also affects immune function by promoting a pro-inflammatory TME milieu. We hypothesized miR-15a inhibition will increase tumor cell death through preservation of EC SMPD1, enhancing endothelial apoptosis and inflammatory cytokine upregulation. Methods: Using TaqMan Human miR panels, miRs were profiled in human umbilical vein ECs (HUVECs) after single 2 vs 20 Gy treatment. miR-target prediction programs identified miRs targeting SMPD1. In vitro gain and loss of function studies were performed with miR transfections in HUVECs and CT26 CRC cells. CXCL10 expression was measured by qRT-PCR. Caspase 1 activation was measured by a luminescence based assay. A CT26 syngeneic CRC flank murine model was used for in vivo miR-15a inhibitor assessment administered via tail vein injection unencapsulated or encapsulated in vascular-targeted 7C1 nanoparticles. Results: Among miRs targeting SMPD1, miR-15a exhibited the greatest differential change in HUVECs 6h post-IR between low and high dose radiation. Lower dose was associated with higher miR-15a and vice versa. Further, miR-15a levels inversely correlated with SMPD1. Exogenous miR-15a significantly decreased SMPD1 mRNA and protein. miR-15a inhibition decreased proliferation in both HUVECs and CT26 cells and increased apoptosis when combined with radiation. miR-15a inhibition increased endothelial CXCL10 expression and caspase-1 activation. Both systemic and vascular-targeted miR-15a inhibitor significantly diminished tumor growth in vivo. Conclusions: Our data suggests inhibition of vascular miR-15a is sufficient to decrease tumor growth likely due to rescue of endothelial SMPD1.

Reduction-responsive core-crosslinked hyaluronic acid-b-poly(trimethylene carbonate-co-dithiolane trimethylene carbonate) micelles: synthesis and CD44-mediated potent delivery of docetaxel to triple negative breast tumor in vivo

2018 ◽  
Vol 6 (19) ◽  
pp. 3040-3047 ◽  
Author(s):  
Yaqin Zhu ◽  
Jian Zhang ◽  
Fenghua Meng ◽  
Liang Cheng ◽  
Jan Feijen ◽  
...  
Keyword(s):  
Hyaluronic Acid ◽  
Tumor Growth ◽  
Breast Tumor ◽  
Triple Negative ◽  
Trimethylene Carbonate ◽  
Inhibit Tumor Growth

Docetaxel-loaded core crosslinked HA-P(TMC-DTC) micelles show high targetability to CD44-overexpressing MDA-MB-231 breast tumor and effectively inhibit tumor growth.

scholarly journals Suppression of in vivo tumor growth and induction of suspension cell death by tissue inhibitor of metalloproteinases (TIMP)-3

1996 ◽  
Vol 17 (9) ◽  
pp. 1805-1811 ◽  
Author(s):  
Junhui Bian ◽  
Yuli Wang ◽  
Mark R. Smith ◽  
Hyungtae Kim ◽  
Christine Jacobs ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Growth ◽  
Suspension Cell ◽  
Tissue Inhibitor Of Metalloproteinases ◽  
Tissue Inhibitor

scholarly journals The Disulfiram/Copper Complex Induces Autophagic Cell Death in Colorectal Cancer by Targeting ULK1

2021 ◽  
Vol 12 ◽  
Author(s):  
Yeting Hu ◽  
Yucheng Qian ◽  
Jingsun Wei ◽  
Tian Jin ◽  
Xiangxing Kong ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Death ◽  
Therapeutic Strategy ◽  
Whole Genome ◽  
Library Screening ◽  
Inhibit Tumor Growth ◽  
Squamous Cells ◽  
Novel Therapeutic

Colorectal cancer (CRC) is highly prevalent worldwide, but there has been limited development of efficient and affordable treatment. Induced autophagy has recently been recognized as a novel therapeutic strategy in cancer treatment, and disulfiram (DSF), a well-known antialcohol drug, is also found to inhibit tumor growth in various malignancies. Recently, DSF has been reported to induce excessive autophagy in oral squamous cells; however, little is known about whether it can induce autophagy and suppress proliferation in CRC. In this study, we investigate the effect of DSF with copper (DSF/Cu) on CRC both in vitro and in vivo and find that the combination significantly inhibits CRC cell viability and mainly induces autophagy instead of apoptosis. Furthermore, we use whole genome CRISPR library screening and identify a new mechanism by which DSF triggers autophagy by ULK1. Overall, these findings provide a potential CRC treatment.

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